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Chapter 2
Primary Effects of CNS Trauma
Primary head injuries are defined as those that occur
at the time of initial trauma even though they may
not be immediately apparent on initial evaluation.
Head injury can be caused by direct or indirect trauma. Direct trauma involves a blow to the head and is usually caused by automobile collisions, falls, or injury inflicted by an object such as a hammer or baseball bat. Scalp lacerations, hematomas, and skull fractures are common. Associated intracranial damage ranges from none to severe.
Significant forces of acceleration/deceleration, linear translation, and rotational loading can be applied to the brain without direct head blows. Such indirect trauma is caused by angular kinematics and typically occurs in high-speed motor vehicle collisions (MVCs). Here the brain undergoes rapid deformation and distortion. Depending on the site and direction of the force applied, significant injury to the cortex, axons, penetrating blood vessels, and deep gray nuclei may occur. Severe brain injury can occur in the absence of skull fractures or visible scalp lesions.
We begin our discussion with a consideration of scalp and skull lesions as we work our way from the outside to the inside of the skull. We then delineate the spectrum of intracranial trauma, starting with extraaxial hemorrhages. We conclude this chapter with a detailed discussion of injuries to the brain parenchyma (e.g., cortical contusion, diffuse axonal injury, and the serious deep subcortical injuries).
Scalp and Skull Injuries
Scalp and skull injuries are common manifestations of cranial trauma. Although brain injury is usually the most immediate concern in managing traumatized patients, superficial lesions such as scalp swelling and focal hematoma can be helpful in identifying the location of direct head trauma. On occasion, these initially innocent-appearing "lumps and bumps" can become life-threatening. Before turning our attention to intracranial traumatic lesions, we therefore briefly review scalp and skull injuries, delineating their typical imaging findings and clinical significance.
Scalp Injuries
Scalp injuries include lacerations and hematomas. Scalp lacerations can occur in both penetrating and closed head injuries. Lacerations may extend partially or entirely through all five layers of the scalp (skin, subcutaneous fibrofatty tissue, galea aponeurotica, loose areolar connective tissue, and periosteum) to the skull (2-1).
Focal discontinuity, soft tissue swelling, and subcutaneous air are commonly identified in scalp lacerations. Scalp lacerations should be carefully evaluated
Scalp and Skull Injuries 13 Scalp Injuries 13 Facial Injuries 16 Skull Fractures 16
Extraaxial Hemorrhages 21 Arterial Epidural Hematoma 21 Venous Epidural Hematoma 23 Acute Subdural Hematoma 26 Subacute Subdural Hematoma 29 Chronic/Mixed Subdural Hematoma 32 Traumatic Subarachnoid Hemorrhage 35
Parenchymal Injuries 38 Cerebral Contusions and Lacerations 38 Diffuse Axonal Injury 42 Diffuse Vascular Injury 45 Subcortical (Deep Brain) Injury 47
Miscellaneous Injuries 48 Pneumocephalus 48 Abusive Head Trauma (Child Abuse) 53 Missile and Penetrating Injuries 60
Trauma
(2-4B) Coronal scan in the same case shows the small right ſt, large left- sided cephalohematomas st. The elevated periosteum clearly separates the two blood collections. (2-4C) Sagittal scan reformatted from the axial data shows that the left parietal cephalohematoma st does not cross the coronal suture .
(2-3) Graphic shows the skull of a newborn, including the anterior fontanelle, coronal, metopic, sagittal sutures. Cephalohematoma is subperiosteal, limited by sutures. Subgaleal hematoma is under the scalp aponeurosis, not bounded by sutures. (2- 4A) NECT scan in a newborn shows a small right ſt and a large left st parietal cephalohematoma. Neither crosses the sagittal suture .
(2-1) Coronal graphic depicts normal layers of the scalp. Skin, subcutaneous fibrofatty tissue overlie the galea aponeurotica , loose areolar connective tissue. The pericranium is the periosteum of the skull and continues into and through sutures to merge with the periosteal layer of the dura . (2-2) NECT shows scalp laceration st, hyperdense foreign bodies ſt, and subgaleal air .
Trauma
Subgaleal hematomas are subaponeurotic collections and are common findings in traumatized patients of all ages. Here blood collects under the aponeurosis (the "galea") of the occipitofrontalis muscle (2-5). Because a subgaleal hematoma lies deep to the scalp muscles and galea aponeurotica but external to the periosteum, it is not anatomically limited by suture lines.
Bleeding into the subgaleal space can be very extensive. Subgaleal hematomas are usually bilateral lesions that often spread diffusely around the entire calvaria. NECT scans show a heterogeneously hyperdense crescentic scalp mass that crosses one or more suture lines (2-6).
Most subgaleal hematomas resolve without treatment. In contrast to benign self-limited cephalohematomas, however, expanding subgaleal hematomas in infants and small children can cause significant blood loss.
Facial Injuries
Facial fractures are commonly overlooked on initial imaging (typically head CT scans). Important soft tissue markers can be identified that correlate with facial fractures and may merit a dedicated CT evaluation of the facial bones. These include periorbital contusions and subconjunctival hemorrhage as well as lacerations of the lips, mouth, and nose.
Holmgren et al. (2005) have proposed the mnemonic LIPS-N (lip laceration, intraoral laceration, periorbital contusion, subconjunctival hemorrhage, and nasal laceration) be used in conjunction with physical examination. If any of these is present, a traumatized patient should have a dedicated facial CT in addition to the standard head CT.
Skull Fractures
Noticing a scalp "bump" or hematoma on initial imaging in head trauma is important, as calvarial fractures rarely—if
(2-10B) Coronal bone CT reformatted from the axial source data in the same case shows that the depressed skull fracture is near the midline, raising concern for superior sagittal sinus injury. (2-10C) Sagittal bone CT in the same case shows the depressed skull fracture , associated with a focal scalp hematoma st. CTV (not shown) demonstrated SSS narrowing without occlusion or venous EDH.
(2-9) 3D shaded surface display (SSD) in a patient with multiple linear and diastatic skull fractures shows utility of SSDs in depicting complex fracture anatomy. Note slight depression of the fractured parieto- occipital calvarium. (2- 10A) Axial bone CT in a patient who was hit in the head with a falling ladder shows an extensively comminuted, depressed skull fracture .
Primary Effects of CNS Trauma
ever—occur in the absence of overlying soft tissue swelling or scalp laceration. Skull fractures are present on initial CT scans in about two-thirds of patients with moderate head injury, although 25-35% of severely injured patients have no identifiable fracture even with thin-section bone reconstructions.
Skull fractures can be simple or comminuted, closed or open. In open fractures, skin laceration results in communication between the external environment and intracranial cavity. Infection risk is high in this type of fracture, as it is with fractures that cross the mastoids and paranasal sinuses.
Several types of acute skull fracture can be identified on imaging studies: linear, depressed, elevated, and diastatic fractures (2-7). Fractures can involve the calvaria, skull base, or both. Another type of skull fracture, a "growing" skull fracture, is a rare but important complication of skull trauma.
Linear Skull Fractures
A linear skull fracture is a sharply marginated linear defect that typically involves both the inner and outer tables of the calvaria (2-8).
Most linear skull fractures are caused by relatively low-energy blunt trauma that is delivered over a relatively wide surface area. Linear skull fractures that extend into and widen a suture become diastatic fractures (see below). When multiple complex fractures are present, 3D shaded surface display (SSD) can be very helpful in depicting their anatomy and relationships to cranial sutures.
Patients with an isolated linear nondisplaced skull fracture (NDSF), no intracranial hemorrhage or pneumocephalus, normal neurologic examination, and absence of other injuries are at very low risk for delayed hemorrhage or other life- threatening complication. Hospitalization is not necessary for many children with NDSFs.
(2-12A) Axial NECT scan in a 20y man who had a tree fall on his head shows a massive subgaleal hematoma crossing the anterior aspect of the sagittal suture ſt. A small extraaxial hematoma st, most likely a venous epidural hematoma, is present. (2-12B) Bone CT in the same case shows a diastatic fracture of the sagittal suture ſt. Nondisplaced linear fractures are also present.
(2-11A) Axial NECT scan shows severe scalp laceration with a combination of elevated st, depressed skull fractures. (2-11B) Bone CT in the same case shows that the elevated fracture is literally "hinged" away from the calvaria.
Primary Effects of CNS Trauma
erosion," is a rare lesion that occurs in just 0.3-0.5% of all skull fractures (2- 13). Most patients with GSF are under 3 years of age.
GSFs develop in stages and slowly widen over time. In the first "prephase," a skull fracture (typically a linear or comminuted fracture) lacerates the dura, and brain tissue or arachnoid membrane herniates through the torn dura. Stage I extends from the time of initial injury to just before the fracture enlarges. Early recognition and dural repair of stage I GSFs produce the best results.
Stage II is the early phase of GSF. Stage II lasts for approximately 2 months following initial fracture enlargement. At this stage, the bone defect is small, the skull deformity is relatively limited, and neurologic deficits are mild. Nevertheless, the entrapped tissue prevents normal fracture healing.
Stage III represents late-stage GSF and begins 2 months after the initial enlargement begins. During this stage, the bone defect becomes significantly larger. Brain tissue and CSF extend between the bony edges of the fracture through torn dura and arachnoid.
Patients with late-stage GSFs often present months or even years after head trauma. Stage III GSFs can cause pronounced skull deformities and progressive neurologic deficits if left untreated.
Imaging
General Features. Plain skull radiographs have no role in the modern evaluation of traumatic head injury. One-quarter of patients with fatal brain injuries have no skull fracture at autopsy. CT is fast, widely available, sensitive for both bone and brain injury, and the worldwide diagnostic standard of care for patients with head injuries. New generations of multislice CT scanners offer very short acquisition times with excellent spatial resolution.
Both bone and soft tissue reconstruction algorithms should be used when evaluating patients with head injuries. Soft tissue reconstructions should be viewed with both narrow ("brain") and intermediate ("subdural") windows. Coronal and sagittal reformatted images obtained using the axial source data are helpful additions.
Three-dimensional reconstruction and curved MIPs of the skull have been shown to improve fracture detection over the use of axial sections alone.
CT Findings. While fractures can involve any part of the calvaria or skull base, the middle cranial fossa is most susceptible because of its thin "squamous" bones and multiple foramina and fissures.
NECT scans demonstrate linear skull fractures as sharply marginated lucent lines. Depressed fractures are typically comminuted and show inward implosion of fracture fragments (2-10). Elevated fractures show an elevated, rotated skull segment (2-11). Diastatic fractures appear as widened sutures or synchondroses (2-14) (2-15) and are usually associated with linear skull fractures.
Stage I " growing" fractures are difficult to detect on initial NECT scans, as scalp and contused brain are similar in density. Identifying torn dura with herniated brain tissue is similarly difficult although cranial ultrasound can be more helpful.
Later-stage GSFs demonstrate a progressively widening and unhealing fracture. A lucent skull lesion with rounded, scalloped margins and beveled edges is typical (2-13). CSF and soft tissue are entrapped within the expanding fracture. Most GSFs are directly adjacent to posttraumatic encephalomalacia, so the underlying brain often appears hypodense.
(2-15B) CT in the same case shows carotid arteries ſt, sigmoid sinuses are patent. A small right venous EDH st is present.
(2-15A) Linear ſt, diastatic fractures of the skull base are present crossing the jugular foramen st, both carotid canals .
(2-14) Autopsy shows multiple skull base fractures involving clivus ſt, carotid canals , jugular foramina st. (E. T. Hedley-White, MD.)
Trauma
(2-17B) Dorsal view of the dura-covered brain shows the biconvex EDH ſt on top of the dura. (Courtesy E. T. Hedley-Whyte, MD.)
(2-17A) Endocranial view shows temporal bone fracture crossing the middle meningeal artery groove st. Note biconvex margins of EDH .
(2-16) Graphic shows EDH , depressed skull fracture lacerating middle meningeal artery st. Inset shows rapid bleeding, "swirl" sign ſt.
MR Findings. MR is rarely used in the setting of acute head trauma because of high cost, limited availability, and lengthy time required. Compared with CT, bone detail is poor although parenchymal injuries are better seen. Adding T2* sequences, particularly SWI, is especially helpful in identifying hemorrhagic lesions.
In some cases, MR may be indicated for early detection of potentially treatable complications. A young child with neurologic deficits or seizures, a fracture larger than 4 millimeters, or a soft tissue mass extending through the fracture into the subgaleal space is at risk for developing a GSF. MR can demonstrate the dural tear and differentiate herniated brain from contused, edematous scalp.
Angiography. If a fracture crosses the site of a major vascular structure such as the carotid canal or a dural venous sinus (2-14), CT angiography is recommended. Sagittal, coronal, and MIP reconstructions help delineate the site and extent of vascular injuries.
Clival and skull base fractures are strongly associated with neurovascular trauma, and CTA should always be obtained in these cases (2-15). Cervical fracture dislocations, distraction injuries, and penetrating neck trauma also merit further investigation. Uncomplicated asymptomatic soft tissue injuries of the neck rarely result in significant vascular injury.
SCALP AND SKULL INJURIES
Scalp Injuries
- Lacerations ○± Foreign bodies
- Cephalohematoma ○Usually infants ○Subperiosteal ○Small, unilateral (limited by sutures)
- Subgaleal hematoma ○Between galea, periosteum of skull ○Circumferential, not limited by sutures ○Can be very large, life-threatening Skull Fractures
- Linear ○Sharp lucent line ○Can be extensive and widespread
- Depressed ○Focal ○Inwardly displaced fragments ○Often lacerates dura-arachnoid
- Elevated ○Rare ○Fragmented rotated outward
- Diastatic ○Typically associated with severe trauma ○Usually caused by linear fracture that extends into suture ○Widens, spreads apart suture or synchondrosis
- "Growing" ○Rare ○Usually in young children ○Fracture lacerates dura-arachnoid ○Brain/arachnoid herniates through torn dura ○Trapped tissue prevents bone healing ○CT: Rounded edges, scalloped margins of skull ○MR: CSF ± brain
Trauma
(2-20C) Repeat study 6 weeks after trauma reveals that the EDH has resolved completely.
(2-20B) Repeat scan 10 days later reveals that density of the EDH has decreased significantly.
(2-20A) Serial imaging demonstrates temporal evolution of a small nonoperated EDH. Initial NECT scan shows a hyperdense biconvex EDH .
Demographics. EDHs are uncommon in infants and the elderly. Most are found in older children and young adults. The M:F ratio is 4:1.
Presentation. The prototypical "lucid interval," during which a traumatized patient has an initial brief loss of consciousness followed by an asymptomatic period of various length prior to onset of coma and/or neurologic deficit, occurs in only 50% of EDH cases. Headache, nausea, vomiting, symptoms of intracranial mass effect (e.g., pupil-involving third cranial nerve palsy) followed by somnolence and coma are common.
Natural History. Outcome depends on size and location of the hematoma, whether the EDH is arterial or venous, and whether there is active bleeding (see below). In the absence of other associated traumatic brain injuries, overall mortality rate with prompt recognition and appropriate treatment is under 5%.
Delayed development or enlargement of an EDH occurs in 10-15% of cases, usually within 24-36 hours following trauma.
Treatment Options. Many EDHs are now treated conservatively. Most traumatic EDHs are not surgical lesions at initial presentation, and the rate of conversion to surgery is low. Most venous and small classic hyperdense EDHs that do not exhibit a "swirl" sign and have minimal or no mass effect are managed conservatively with close clinical observation and follow-up imaging (2-20). Significant clinical predictors of EDH progression requiring conversion to surgical therapy are coagulopathy and younger age.
Imaging
General Features. EDHs, especially in adults, typically do not cross sutures unless a fracture with sutural diastasis is present. In children, 10% of EDHs cross suture lines, usually the coronal or sphenosquamous suture.
Look for other comorbid lesions such as "contre-coup" injuries, tSAH, and secondary brain herniations, all of which are common findings in patients with EDHs.
CT Findings. NECT scan is the procedure of choice for initial imaging in patients with head injury. Both soft tissue and bone reconstruction algorithms should be obtained. Multiplanar reconstructions are especially useful in identifying vertex EDHs, which may be difficult to detect if only axial images are obtained.
The classic imaging appearance of classic (arterial) EDHs is a hyperdense (60-90 HU) biconvex extraaxial collection (2-18). Presence of a hypodense component ("swirl" sign) is seen in about one-third of cases and indicates active, rapid bleeding with unretracted clot (2-16) (2-19).
EDHs compress the underlying subarachnoid space and displace the cortex medially, "buckling" the gray-white matter interface inward.
Air in an EDH occurs in approximately 20% of cases and is usually—but not invariably—associated with a sinus or mastoid fracture.
Patients with mixed-density EDHs tend to present earlier than patients with hyperdense hematomas and have lower Glasgow Coma Scores (GCSs), larger hematoma volumes, and poorer prognosis.
Imaging findings associated with adverse clinical outcome are thickness > 1. cm, volume > 30 mL, pterional (lateral aspect of the middle cranial fossa) location, midline shift > 5 mm, and presence of a "swirl sign" within the hematoma on imaging.
Primary Effects of CNS Trauma
MR Findings. Acute EDHs are typically isointense with underlying brain, especially on T1WI. The displaced dura can be identified as a displaced "black line" between the hematoma and the brain.
Angiography. DSA may show a lacerated middle meningeal artery with "tram-track" fistulization of contrast from the middle meningeal artery into the paired middle meningeal veins. Mass effect with displaced cortical arteries and veins is seen.
CLASSIC ACUTE EPIDURAL HEMATOMA
Terminology
- EDH = blood between skull, dura Etiology
- Associated skull fracture in 90-95%
- Arterial 90% ○Most often middle meningeal artery
- Venous 10% Pathology
- Unilateral, supratentorial (> 90%)
- Dura stripped away from skull → biconvex hematoma
- Usually does not cross sutures (exception = children, 10%)
- Does cross sites of dural attachment Clinical
- Rare (1-4% of head trauma)
- Older children, young adults most common
- M:F = 4:
- Classic "lucid interval" in only 50%
- Delayed deterioration common
- Low mortality if recognized, treated
- Small EDHs ○If minimal mass, no "swirl sign" often managed conservatively Imaging
- Hyperdense lens-shaped
- "Swirl sign" (hypodensity) = rapid bleeding
Venous Epidural Hematoma
Not all EDHs are the same!! Venous EDHs are often smaller, are under lower pressure, and develop more slowly than their arterial counterparts. Most venous EDHs are caused by a skull fracture that crosses a dural venous sinus and therefore occur in the posterior fossa near the skull base (transverse/sigmoid sinus) (2-21) or the vertex of the brain (superior sagittal sinus). In contrast to their arterial counterparts, venous EDHs can "straddle" intracranial compartments, crossing both sutures and lines of dural attachment (2-22) and compressing or occluding the adjacent venous sinuses.
Venous EDHs can be subtle and easily overlooked. Coronal and sagittal reformatted images are key to the diagnosis and delineation of these variant EDHs (2-23). Several anatomic subtypes of venous EDHs, each with different treatment implications and prognosis, are recognized.
Vertex EDH
"Vertex" EDHs are rare. Usually caused by a linear or diastatic fracture that crosses the superior sagittal sinus, they often accumulate over hours or even days with slow, subtle onset of symptoms (2-24). "Vertex" hematomas can be subtle and are easily overlooked unless coronal and sagittal reformatted images are obtained.
(2-23) (L) Coronal, (R) sagittal CTV shows venous EDH straddling the tentorium ſt, elevating the left transverse sinus st.
(2-22) Autopsy shows that venous EDH caused by transverse sinus injury "straddles" the tentorium ſt. (Courtesy R. Hewlett, MD.)
(2-21) Graphic shows basilar skull fracture with transverse sinus occlusion and posterior fossa venous EDH st.
Primary Effects of CNS Trauma
(2-27A) Axial CTA in a child with craniovertebral junction trauma shows a small clival EDH . There was no evidence for vascular injury. (2-27B) Sagittal CTA reformatted from the axial source date nicely demonstrates the clival epidural hematoma .
(2-26B) Axial bone CT in the same case shows a fracture through the right greater sphenoid wing ſt. (2-26C) CT venogram in the same case shows a displaced, lacerated sphenoparietal sinus with contrast extravasation ("spot sign") st. Note the EDH is limited medially by the orbital fissure . The patient was treated nonsurgically. The EDH showed no further enlargement and resolved completely.
(2-25) Graphic depicts benign anterior temporal epidural hematoma. Fracture ſt disrupts the sphenoparietal sinus . Low-pressure venous EDH is anatomically limited, medially by the orbital fissure st and laterally by the sphenotemporal suture . (2-26A) Axial NECT in a 33y man with head trauma shows a biconvex anterior temporal acute epidural hematoma .
Trauma
(2-30) NECT scan shows that small SDH ſt is easier to see with wider (R) compared with standard (L) windows.
(2-29) Acute SDH spreads over left hemisphere ſt, along tentorium , into interhemispheric fissure st but does not cross midline.
(2-28) Graphic depicts crescent-shaped acute SDH st with contusions and "contre-coup" injuries , diffuse axonal injuries .
minor cranial nerve involvement, the clinical course is usually benign, and treatment with a cervical collar is typical.
NECT scans show a hyperdense collection between the clivus and tectorial membrane. Sagittal MR of the craniocervical junction shows the hematoma elevating the clival dura and extending inferiorly between the basisphenoid and tectorial membrane anterior to the medulla.
Acute Subdural Hematoma
Acute subdural hematomas (aSDHs) are one of the leading causes of death and disability in patients with severe traumatic brain injury. SDHs are much more common than EDHs. Most do not occur as isolated injuries; the vast majority of SDHs are associated with traumatic subarachnoid hemorrhage (tSAH) as well as significant parenchymal injuries such as cortical contusions, brain lacerations, and diffuse axonal injuries.
Terminology
An aSDH is a collection of acute blood products that lies in or between the inner border cell layer of the dura and the arachnoid (2-28).
Etiology
Trauma is the most common cause of aSDH. Both direct blows to the head and nonimpact injuries may result in formation of an aSDH. Tearing of bridging cortical veins as they cross the subdural space to enter a dural venous sinus (usually the superior sagittal sinus) is the most common etiology. Cortical vein lacerations can occur with either a skull fracture or the sudden changes in velocity and brain rotation that occur during nonimpact closed head injury.
Blood from ruptured vessels spreads quickly through the potential space between the dura and the arachnoid. Large SDHs may spread over an entire hemisphere, extending into the interhemispheric fissure and along the tentorium.
Tearing of cortical arteries from a skull fracture may also give rise to an aSDH. The arachnoid itself may also tear, creating a pathway for leakage of CSF into the subdural space, resulting in admixture of both blood and CSF.
Less common causes of aSDH include aneurysm rupture, skull/dura- arachnoid metastases from vascular extracranial primary neoplasms, and spontaneous hemorrhage in patients with severe coagulopathy.
Rarely, an acute spontaneous SDH of arterial origin occurs in someone without any traumatic history or vascular anomaly. These patients usually have sudden serious disturbance of consciousness and have a poor outcome unless the aSDH is recognized and treated promptly.
Pathology
Gross Pathology. The gross appearance of an aSDH is that of a soft, purplish, "currant jelly" clot beneath a tense bulging dura. More than 95% are supratentorial. Most aSDHs spread diffusely over the affected hemisphere and are therefore typically crescent-shaped.
Clinical Issues
Epidemiology. An aSDH is the second most common extraaxial hematoma, exceeded only by tSAH. An aSDH is found in 10-20% of all patients with head injury and is observed in 30% of autopsied fatal injuries.
Trauma
quickly. Here the mass effect is greatly disproportionate to the size of the SDH, which may be relatively small.
Occasionally, an aSDH is nearly isodense with the underlying cortex. This unusual appearance is found in extremely anemic patients (Hgb under 8-10 g/dL) (2-36) and sometimes occurs in patients with coagulopathy. In rare cases, CSF leakage through a torn arachnoid may mix with—and dilute—the acute blood that collects in the subdural space.
CECT. CECT scans are helpful in detecting small isodense aSDHs. The normally enhancing cortical veins are displaced inward by the extraaxial fluid collection.
Perfusion CT. CT or xenon perfusion scans may demonstrate decreased cerebral blood flow (CBF) and low perfusion pressure, which is one of the reasons for the high mortality rate of patients with aSDHs. The cortex underlying an evacuated aSDH may show hyperemic changes with elevated
rCBF values. Persisting hyperemia has been associated with poor outcome.
MR Findings. MR scans are rarely obtained in acutely brain- injured patients. In such cases, aSDHs appear isointense on T1WI and hypointense on T2WI. Signal intensity on FLAIR scans is usually iso- to hyperintense compared with CSF but hypointense compared with the adjacent brain. aSDHs are hypointense on T2* scans.
DWI shows heterogeneous signal within the hematoma but may show patchy foci of restricted diffusion in the cortex underlying the aSDH.
Angiography. CTA may be useful in visualizing a cortical vessel that is actively bleeding into the subdural space.
(2-35) NECT shows a mixed-density 12-mm aSDH with a disproportionately large subfalcine herniation of the lateral ventricles ( mm), indicating that diffuse holohemispheric brain swelling is present. Subfalcine herniation ≥ 3 mm portends a poor prognosis. (2-36) NECT scan in a very anemic patient shows an isodense aSDH . The aSDH is almost exactly the same density as the underlying cortex. The gray-white interface is displaced inward .
(2-33) (L) Initial NECT in an anticoagulated male patient shows a small mixed-density SDH. (R) Scan 6 hours later shows expanding, actively bleeding aSDH. (2-34) NECT scan shows a 55y man with an actively hemorrhaging aSDH. Some clotted blood is present ſt, but much of the hematoma consists of isodense unclotted hemorrhage .
Primary Effects of CNS Trauma
Differential Diagnosis
In the setting of acute trauma, the major differential diagnosis is EDH. Shape is a helpful feature, as most aSDHs are crescentic, whereas EDHs are biconvex. EDHs are almost always associated with skull fracture; SDHs frequently occur in the absence of skull fracture. EDHs may cross sites of dural attachment; SDHs do not cross the falx or tentorium.
Subacute Subdural Hematoma
With time, subdural hematomas (SDHs) undergo organization, lysis, and neomembrane formation. Within 2-3 days, the initial soft, loosely organized clot of an acute SDH becomes organized. Breakdown of blood products and the formation of organizing granulation tissue change the imaging appearance of subacute and chronic SDHs.
Terminology
A subacute subdural hematoma (sSDH) is between several days and several weeks old.
Pathology
A collection of partially liquified clot with resorbing blood products is surrounded on both sides by a "membrane" of organizing granulation tissue (2-37). The outermost membrane adheres to the dura and is typically thicker than the inner membrane, which abuts the thin, delicate arachnoid (2-38).
In some cases, repetitive hemorrhages of different ages arising from the friable granulation tissue may be present. In others, liquefaction of the hematoma over time produces serous blood-tinged fluid.
Clinical Issues
Epidemiology and Demographics. SDHs are common findings at imaging and autopsy. In contrast to acute SDHs, sSDHs show a distinct bimodal distribution with children and the elderly as the most commonly affected age groups.
Presentation. Clinical symptoms vary from asymptomatic to loss of consciousness and hemiparesis caused by sudden rehemorrhage into an sSDH. Headache and seizure are other common presentations.
Natural History and Treatment Options. Many sSDHs resolve spontaneously. In some cases, repeated hemorrhages may cause sudden enlargement and mass effect. Surgical drainage may be indicated if the sSDH is enlarging or becomes symptomatic.
Imaging
General Features. Imaging findings are related to hematoma age and the presence of encasing membranes. Evolution of an untreated, uncomplicated SDH follows a very predictable pattern on CT. Density of an extraaxial hematoma decreases approximately 1-2 HU each day (2-39). Therefore, an SDH will become nearly isodense with the underlying cerebral cortex within a few days following trauma.
CT Findings. sSDHs are typically crescent-shaped fluid collections that are iso- to slightly hypodense compared with the underlying cortex on NECT (2- 40). Medial displacement of the gray-white interface ("buckling") is often present, along with "dot-like" foci of CSF in the trapped, partially effaced sulci underlying the sSDH (2-41) (2-42). Mixed-density hemorrhages are common.
(2-39) SDHs decrease approximately 1.5 HU/day. By 7-10 days, blood in hematoma is isodense with cortex. By 10 days, it is hypodense.
(2-38) Autopsy shows sSDH with organized hematoma ſt, thick outer membrane st, deformed brain . (Courtesy R. Hewlett, MD.)
(2-37) Graphic depicts sSDH ſt. Inset shows bridging vein and thin inner and thick outer membranes.
Primary Effects of CNS Trauma
Bilateral sSDHs may be difficult to detect because of their "balanced" mass effect (2-41). Sulcal effacement with displaced gray-white matter interfaces is the typical appearance.
CECT scans show that the enhanced cortical veins are displaced medially. The encasing membranes, especially the thicker superficial layer, may enhance.
MR Findings. MR can be very helpful in identifying sSDHs, especially small lesions that are virtually isodense with underlying brain on CT scans.
Signal intensity varies with hematoma age but is less predictable than on CT, making precise "aging" of subdural collections more problematic. In general, early subacute SDHs are isointense with cortex on T1WI and hypointense on T2WI but gradually become more hyperintense as extracellular methemoglobin increases (2-43A). Most late-stage sSDHs are T1/T2 "bright-bright." A linear T2 hypointensity representing
the encasing membranes that surround the SDH is sometimes present.
FLAIR is the most sensitive standard sequence for detecting sSDH, as the collection is typically hyperintense (2-44). Because FLAIR signal intensity varies depending on the relative contribution of T1 and T2 effects, early sSDHs may initially appear hypointense due to their intrinsic T shortening.
T2* scans are also very sensitive, as sSDHs show distinct "blooming" (2-43B).
Signal intensity on DWI also varies with hematoma age. DWI commonly shows a crescentic high-intensity area with a low- intensity rim closer to the brain surface ("double layer" appearance) (2-43C). The low-intensity area corresponds to a mixture of resolved clot and CSF, whereas the high-intensity area correlates with solid clot.
(2-44C) The fluid collections ſt do not suppress on FLAIR and are hyperintense to CSF in the underlying cisterns. (2- 44D) T1 C+ shows that the outer membrane of the SDH enhances ſt. Findings are consistent with late subacute/early chronic subdural hematomas.
(2-44A) T1WI in a 59y man with seizures shows bilateral subdural collections ſt that are slightly hyperintense to CSF. (2-44B) T2WI shows that both collections ſt are isointense with CSF in the underlying subarachnoid cisterns.
Trauma
(2-47) cSDH autopsy has thickened dura 1 side ſt, mixed acute, subacute, chronic hemorrhages on other . (DP: Hospital Autopsy.)
(2-46) Complicated cSDHs contain loculated pockets of old and new blood, seen as fluid-fluid levels ſt within septated cavities.
(2-45) Simple cSDHs contain serosanguineous fluid with hematocrit effect, thin inner , thick outer encapsulating membranes.
T1 C+ scans demonstrate enhancing, thickened, encasing membranes (2- 44D). The membrane surrounding an sSDH is usually thicker on the dural side of the collection. Delayed scans may show gradual "filling in" and increasing hyperintensity of the sSDH.
Differential Diagnosis
The major differential diagnosis of an sSDH is an isodense acute SDH. These are typically seen only in an extremely anemic or anticoagulated patient. A subdural effusion that follows surgery or meningitis or that occurs as a component of intracranial hypotension can also mimic an sSDH. A subdural hygroma is typically isodense/isointense with CSF and does not demonstrate enhancing, encapsulating membranes.
Chronic/Mixed Subdural Hematoma
Terminology
A chronic subdural hematoma (cSDH) is an encapsulated collection of sanguineous or serosanguineous fluid confined within the subdural space. Recurrent hemorrhage(s) into a preexisting cSDH are common and produce a mixed-age or "acute on chronic" SDH (mSDH).
Etiology
With continued degradation of blood products, an SDH becomes progressively more liquified until it is largely serous fluid tinged with blood products (2-45). Rehemorrhage, either from vascularized encapsulating membranes or rupture of stretched cortical veins crossing the expanded subdural space, occurs in 5-10% of cSDHs and is considered "acute-on- chronic" SDH (2-46).
Pathology
Gross Pathology. Blood within the subdural space incites tissue reaction around its margins. Organization and resorption of the hematoma contained within the "membranes" of surrounding granulation tissue continue. These neomembranes have fragile, easily disrupted capillaries and easily rebleed, creating an mSDH. Multiple hemorrhages of different ages are common in mSDHs (2-47).
Eventually, most of the liquified clot in a cSDH is resorbed. Only a thickened dura-arachnoid layer remains with a few scattered pockets of old blood trapped between the inner and outer membranes.
Clinical Issues
Epidemiology. Unoperated, uncomplicated subacute SDHs eventually evolve into cSDHs. Approximately 5-10% will rehemorrhage, causing multiloculated mixed-age SDHs.
Demographics. Chronic SDHs may occur at any age. Mixed-age SDHs are much more common in elderly patients.
Presentation. Presentation varies from no/mild symptoms (e.g., headache) to sudden neurologic deterioration if a preexisting cSDH rehemorrhages.
Natural History. In the absence of repeated hemorrhages, cSDHs gradually resorb and largely resolve, leaving a residue of thickened dura-arachnoid that may persist for months or even years. Older patients, especially those with brain atrophy, are subject to repeated hemorrhages.
Treatment Options. If follow-up imaging of a subacute SDH shows expected resorption and regression of the cSDH, no surgery may be
