Which assessment finding in a patient who was admitted the previous day with a basilar skull fracture is most important to report to the health care provider *?

Skull Base Fracture

Fractures of the skull base frequently lead to serious complications, including vascular injuries, cranial nerve palsies, CSF leaks and intra-cranial complications. The skull base is formed by five bones—the occipital, temporal bone, sphenoid bone, cribriform plate of the ethmoid bone and orbital plate of the frontal bone. Furthermore, the skull base can be subdivided into the anterior, central/lateral and posterior skull base. The anterior skull base extends from the orbital plate of the frontal bone to the posterior margin, defined by the lesser wings/body of the sphenoid. The central and lateral skull base is the most complex, given the neurovascular structures that traverse it. It extends from the lesser wings of the sphenoid and anterior clinoid processes to the anterior surface of the temporal bones and dorsum sellae. The central skull base includes the sella and parasellar cavernous sinuses, whilst the lateral skull base includes the petrous and mastoid segments of the temporal bone. The posterior skull base includes the clivus, posterior surface of the temporal bone and occipital bone.

Anterior skull base fractures typically occur with additional cranio­facial fractures of the frontal region and midface. The more complex fractures of the naso-fronto-ethmoidal regions are associated with high risk of CSF leaks and increased risk of meningitis (Fig. 54.9). Anterior skull base fractures can result in disruption of the olfactory pathways and orbitofrontal brain parenchyma and is a common cause of anosmia. Central skull base fractures are typically direct extensions of frontobasal fractures or, less commonly, from fractures of the clivus or posterior fossa. They typically have a sagittal or oblique orientation extending through the sella and sphenoid sinus. Direct trauma to the lateral skull and zygoma can result in a transverse fracture extending through the central skull base. Anterior injuries may involve the orbital apices and optic nerve canals, whilst involvement of the sella can potentially result in disruption of the anterior visual pathways. Fracture complexes involving the orbital apices/fissures and cavernous sinus can result in multiple cranial nerve palsies (cranial nerves III, IV, V1, V2 and VI). Central skull base fractures may disrupt the carotid canals and result in vascular injuries, as described below.

Fractures extending through the lateral part of the middle cranial fossa can involve the temporal bone and these fractures can be subdivided into otic capsule–sparing (most common) and otic capsule–violating fractures. Otic capsule–violating fractures have a significantly increased risk of facial nerve injury, sensorineural hearing impairment and CSF leaks (Fig. 54.10). Fractures that extend through the temporal bone and disrupt the tegmen tympani may be associated with CSF otorrhoea and may result in the development of meningitis and traumatic meningocele (Fig. 54.11).

External Examination

The examination of the nervous system begins with the external appearance of the face, scalp, and neck. Observation and documentation of all injuries to the face, scalp, and neck should be made in a systematic manner. Injuries in the scalp should be examined after shaving the adjacent hair.

Certain external features may be indicative of internal injury, particularly basilar skull fracture, and should direct attention to those sites:

Periorbital ecchymosis is the blue or purple discoloration of the periorbital soft tissues caused by fracture of the overlying orbital plate of the anterior cranial fossa (Figure 1).

Mastoid ecchymosis or the battle sign is blue or purple discoloration over the mastoid area caused by fracture of the petrous portion of the temporal bone.

Blood running from the ear is also caused by fracture of the petrous portion of the temporal bone.

Basilar Skull Fracture

A number of studies have used prophylactic antibiotics in patients with basilar skull fractures and CSF leak on the premise that in patients with a dural defect the CSF is exposed to pathogenic organisms from the nasopharynx, nasal or mastoid sinuses, or external auditory canal.537,538 Interpretation and comparison of the various studies examining this question are confounded by multiple variables, including patient selection, choice of antimicrobial agents, and definition of infection. No prospective controlled trials have examined the efficacy of prophylactic antimicrobial agents in these patients, although a meta-analysis suggested that antibiotic prophylaxis did not prevent meningitis in patients with basilar skull fracture.537 These data have also been analyzed in a Cochrane Database systematic review538 in which prophylactic antibiotic use in patients with basilar skull fracture, whether or not there was evidence of CSF leak, was not supported. However, published studies have biases and randomized controlled trials are needed. Antibiotic use does not appear to change the incidence of posttraumatic bacterial meningitis and may result in the selection and growth of resistant organisms.

Aberrant regeneration

If an oculomotor nerve is injured, recovery may be associated with inappropriate co-contraction (synkinesis) of the extraocular muscles or of the pupil. Possible causes of this include intracranial aneurysm, basilar skull fracture, and neurosurgical operation. There are also rare reports of aberrant regeneration following oculomotor nerve palsies due to diabetes, the Guillain–Barré syndrome, or a midbrain stroke, and it not uncommonly follows congenital oculomotor nerve palsy (Barr et al., 2000; Messé et al., 2001; Georgiou et al., 2003). The synkinesis most commonly involves elevation of the eyelid on downgaze (pseudo Graefe's sign), or contraction of the pupil on adduction. Other synkineses can occur such as lid elevation on attempted adduction or unilateral globe retraction on upgaze or downgaze due to co-contraction of several muscles (Fig. 11.8). Occasionally the contralateral oculomotor nerve or the abducens nerve may be involved (Guy et al., 1989a; Buckley et al., 2005).

Variable degrees of weakness of the muscles supplied by the oculomotor nerve may be present and the pupillary response to light may be reduced or absent. The phenomenon typically occurs about 6 weeks after injury, and the mechanism has therefore been suggested to be one of “miswiring” of axons as they grow back (Sibony et al., 1986).

Basilar Skull Fractures

Basilar fractures are the result of considerable impact force and are highly associated with underlying brain injury. Emergency clinicians should be suspicious of an epidural hematoma in patients with a temporal bone basilar skull fracture. All patients with basilar skull fractures should be admitted for observation, regardless of the need for surgical intervention. A systematic review and meta-analysis of antibiotic prophylaxis following basilar skull fracture has concluded that routine prophylaxis is not supported by the available evidence, whether or not there is evidence of CSF leakage.84,85 We do not recommend routine antibiotics for basilar skull fractures unless the patient is immunocompromised.84,85 Most CSF leaks resolve spontaneously within 1 week, with no complications.98 If the leak persists beyond 7 days, the incidence of bacterial meningitis increases significantly; prophylactic antibiotics should be given in such cases. Antibiotic selection is identical to that for penetrating head trauma. If a patient with a previously diagnosed CSF leak returns to the ED later with fever, the diagnosis of meningitis should be strongly suspected and appropriate evaluation (ie, lumbar puncture) and antibiotic treatment initiated immediately. Treatment of posttraumatic meningitis is discussed inChapter 99.

Cerebrovascular injury

Traumatic vascular injury to the intracranial and extracranial circulation can be the sequelae of blunt or penetrating trauma to the head or neck. These injuries can be difficult to recognize because of the frequent coexistence of traumatic brain injury that can obscure the diagnosis. It is important to identify those patients who may be at risk for a vascular injury, if a stroke is to be prevented.

Blunt extracranial vascular injuries occur most commonly from motor vehicle accidents, mostly involving young patients. The most common mechanism of injury postulated results from stretching of the artery because of rapid deceleration, producing an intimal tear. Some tears probably heal spontaneously, but others lead to dissection, with or without pseudoaneurysm formation, and some thrombose (Larsen, 2002). Other mechanisms of injury include direct blows to the head, neck, or face; strangulation injuries, basilar skull fractures, falls, blunt intraoral trauma, and hyperextension of the neck. A penetrating injury, such as a gunshot wound or stabbing, may injure the common carotid artery, internal carotid artery, or vertebral artery.

Various types of vascular injuries have been identified and include occlusion or thrombosis, dissection, complete transection, pseudoaneurysm, arteriovenous fistula, or a combination of injuries. Bilateral dissections have been reported in up to 45% of patients (Larsen, 2002). A stroke in a patient with a head and neck injury should raise the possibility of a dissection and requires further evaluation.

With a dissection, there is hemorrhage within the vascular wall, typically within the media, that can produce luminal irregularity, stenosis, occlusion, and/or aneurysmal dilatation. Vascular dissection is responsible for 1% of strokes overall, but is responsible for 20% of strokes in young adults (Osborn, 2005).

Traumatic dissections more commonly affect the extracranial vasculature than the intracranial vasculature. In the neck, the internal carotid artery is more frequently involved than the vertebral artery. A dissection of the internal carotid artery can occur a few centimeters above the carotid bifurcation, ending at the skull base (Osborn, 2005). A vertebral artery dissection occurs commonly at the C1–C2 level, where it is most mobile after exiting the foramen transversarium.

Evaluation of a trauma patient suspected of having a cervical dissection includes a noncontrast CT to assess the brain for any associated intracranial injury as well as identify ischemic or embolic sequelae of a vascular injury. Subsequently, a CTA could be performed to evaluate for an abnormal vessel contour, generally considered highly specific and sensitive (Leclerc et al., 1996). Findings of a dissection on CTA include irregular vessel narrowing ± occlusion, tapered stenosis, fusiform aneurysmal dilatation/pseudoaneurysm, “string sign” (long-segment stenosis), intimal flap/double lumen – specific, but rarely seen, and evidence of distal emboli (Fig. 22.35). In the setting of a known cervical spine fracture which can be easily seen on CTA, a careful search should be conducted for an associated vascular injury (Fig. 22.36). Similarly, a CTV could be performed to assess for a dural sinus injury if there is an adjacent fracture. If necessary, the findings on CTA/CTV can be corroborated on conventional angiography.

MRI, magnetic resonance angiography (MRA), and magnetic resonance venography (MRV) are also useful in the detection of an acute infarct or vascular injury in the setting of trauma. MRI findings of a dissection include a T1 hyperintense intramural hematoma, usually eccentric but sometimes circumferential, that surrounds and may narrow the flow void (Figs 22.37 and 22.38). Other findings include the presence of an intimal flap, a thin partition separating the true and false lumens, and a diminished/absent flow void. Like CTV, MRV can assess the integrity of the dural venous sinuses if an adjacent fracture is present. Limitations of MRI are related to the long imaging time and the need for close monitoring of a critically ill trauma patient.

Intracranial vascular trauma may be due to a closed head injury or penetrating skull injury, and may present in a delayed fashion. Traumatic injuries of the intracranial arteries include dissections, aneurysms, and fistulas. These may present individually, or in combination (Larsen, 2002). Traumatic aneurysms account for 1% of intracranial aneurysms.

Carotid-cavernous fistulas (CCFs) are spontaneous or acquired connections between the internal carotid artery and the cavernous sinus. A direct or traumatic CCF is created by a direct connection between the internal carotid artery and the cavernous sinus, resulting from a basal skull fracture with associated laceration of the internal carotid artery or penetrating injury to the head and orbit. Motor vehicle accidents represent the most common cause of traumatic CCFs, followed by trauma from falls and penetrating injuries (Larsen, 2002). Patients with a direct CCF may present with a bruit, pulsating exophthalmos, orbital edema/erythema, decreased vision, glaucoma, and headache. Clinically, these patients may have focal deficits related to cranial nerves III–VI. DSA is required for definitive diagnosis and treatment. However, CT and MRI may suggest the diagnosis. Imaging findings include proptosis, enlargement of the superior ophthalmic vein, cavernous sinus, and extraocular muscles, and reticulation of the intraorbital fat secondary to edema (Fig. 22.39). CT may demonstrate a skull base fracture that may compromise the carotid canal or optic canal. Magnetic resonance angiography may demonstrate increased flow-related signal in the affected cavernous sinus and superior ophthalmic vein, and loss of flow-related signal in the internal carotid artery.

Imaging

The use of appropriate and timely radiographic imaging supplements the clinical exam. Computed tomography (CT) of the head is the gold standard for acute trauma, as it is quickly obtained and provides significant information. Acute hemorrhage on CT is hyperdense and the mass effect on parenchyma can be evaluated. Fractures are seen well on bony windows. Fine cuts on the CT can be utilized to evaluate trauma to intricate temporal bone and skull base structures and guide management. Linear nondisplaced fractures are treated conservatively, but if they overlie important vascular structures they should alert the clinician to possible arterial and venous injury. Examples of these include temporal bone fractures near the middle meningeal artery, and occipital bone fractures over the dural sinuses, both of which can cause EDH (Fig. 113.1). Skull base fractures are often indicative of significant head injury because of the force necessary to fracture thick bone such as the petrous temporal bone. Cranial nerves can be involved if these fractures involve neural foramina or bony casings, such as the facial nerve within the temporal bone. Coronal and 3D reconstructions of source images are useful for depressed skull fractures and operative decision making. Pneumocephalus (intracranial air outside of the sinuses or mastoid air cells) can be seen on bony windows, suggests a mastoid or sinus fracture, and alerts the clinician to look for active or future CSF leak. Loss of a clear sulcal–gyral pattern and effacement of cisterns indicate brain edema, as seen in Figure 113.2. Effacement of ventricles or enlargement of ventricles suggest elevations in ICP from brain edema and hydrocephalus respectively. Contusions have a mixed hyper- and hypodense appearance on CT, as immediate concussive injury is interspersed with necrotic areas that can form hemorrhages over 1–2 days (Fig. 113.3). Significant midline axial shift can be seen with edema or mass occupying lesions, and is more predictive of a poorer outcome than sagittal or vertical displacement.

There are considerations about relative cancer risk from frequent CT scans and its use in pregnant patients. It is common practice in local emergency rooms to obtain a head CT in any patient with reported recent head trauma or fall, but criteria have been proposed to delineate when imaging is warranted and to address unnecessary utilization. The New Orleans criteria (Haydel et al., 2000) were developed to help decide which patients with minor head trauma, normal GCS scores, and normal neurologic exams warranted surveillance CT scans. An increasing number of seven symptoms patients had improved the sensitivity for positive radiographic findings toward 100%: headache, vomiting, age over 60, drug or alcohol intoxication, short-term memory problems, supraclavicular trauma, and seizure. The Canadian CT Head Rule for minor head trauma derived five high-risk factors to predict the likelihood of positive findings: failure to reach a GCS of 15 within 2 hours of injury, open skull fracture, signs of basilar skull fracture such as periorbital ecchymosis, two or more vomiting episodes, or age over 65 (Stiell et al., 2001). These two methods were compared recently, and the Canadian Rule was found to be more specific for predicting neurosurgical intervention (Stiell et al., 2005). In general, CT imaging should be obtained in any patient that has any of the following: loss of consciousness of more than 5 minutes, worsening mental status, seizure, focal deficit, amnesia lasting more than 24 hours, penetrating skull injury, clinical evidence of basal or depressed skull fracture, and significant aggression or confusion.

As already mentioned, there are distinct CT changes that should alert the physician to the severity of TBI, and the possible need for surgical intervention. The Marshall criteria in Table 113.4 outlined early predictors of poor outcome (Marshall et al., 1991, 1992). The criteria have been modified over the years to include several findings that predict a poor outcome in serious TBI. These include obliteration of basal cisterns, significant midline shift, large mass effect-inducing hemorrhages, and significant interventricular blood (Maas et al., 2005). The classification also predicted the severity of TBI, with abnormal CT findings in only 2.5–8% in mild (GCS 13–15) TBI, while 68–94% of severe (GCS < 9) TBI patients have at least one of the findings listed above. Absent basal cisterns may be the most predictive, with a mortality of over 75% (Toutant et al., 1984). A recent study of contusions showed an initial size > 14 mL and presence of a subdural hematoma (correlating to severity of injury) predicted radiographic progression, and up to 20% may require surgical intervention for mass effect (Alahmadi et al., 2010).

Table 113.4. Marshall CT classification of TBI

CategoryDefinitionDiffuse injury INo visible pathology on CT scanDiffuse injury IICisterns are present with midline shift &lt; 5 mm and/or lesion densities present
No high or mixed-density lesion &gt; 25 mL, may include bone fragments and foreign bodiesDiffuse injury IIICisterns compressed or absent with midline shift 0–5 mm
No high or mixed-density lesions &gt; 25 mLDiffuse injury IVMidline shift &gt; 5 mm
No high or mixed-density lesions &gt; 25 mLEvacuated mass lesionAny lesions surgically evacuatedNon-evacuated mass lesionHigh or mixed-density lesion &gt; 25 mL, not surgically evacuated

CT, computed tomography; TBI, traumatic brain injury,

There are modalities within the spectrum of tomographic imaging that provide other useful information. Involvement of the carotid canal in a skull base fracture warrants a CT angiogram (CTA), as carotid dissection occurs in 40% of patients with petrous carotid canal fracture (York et al., 2005). CTA is more effective for identifying wall abnormalities (such as traumatic pseudoaneurysm or dissection) and less invasive than a formal angiogram. CT perfusion imaging allows measurement of CBF and may have some benefit as a supplement to CPP obtained from monitoring, since CPP and CBF autoregulation is altered in TBI (Wintermark et al., 2004). CT perfusion also helps determine the volume of ischemic versus infarcted tissue to guide therapy and provide prognosis. CT spectroscopy (SPECT) can also reveal abnormalities in CBF. A negative post-TBI SPECT has been shown to have some utility in predicting a good long-term outcome (Jacobs et al., 1996).

Other imaging modalities have been used. Magnetic resonance imaging (MRI) is another option in TBI, and is considered to be superior 2–3 days after injury (Lee and Newberg, 2005). It is more sensitive than CT for neuronal damage and stroke, brainstem injury (which CT cannot detect due to skull base beam artifact), as well as smaller multifocal hemorrhages seen in DAI. Hypoxic ischemic injury is easily identified on diffusion-weighted MR sequences. MRI can be helpful to date subdural hematomas, as the changes that occur in T1- and T2-weighted sequences reflect the location and type of hemoglobin in the clot over time (Atlas and Thulborn, 2002). MRI is also more sensitive than CT for picking up small SDHs as is seen in child abuse (Gentry et al., 1988) and for detection of traumatic subarachnoid hemorrhage, especially gradient echo and FLAIR sequences (Wiesmann et al., 2002). It does not use the ionizing radiation of CT, so it is considered safer in children and pregnant patients. Despite its utilities, no relationship has been established between MRI appearance of the brain after traumatic injury and neurologic outcome (Levin et al., 1989). MR arteriography and venography can identify vascular injury, including sinus thrombosis. MR spectroscopy can reveal a reduced N-acetylaspartate/creatinine ratio indicating neuronal loss, but its utility in predicting outcome in TBI remains unclear. Position emission tomography (PET) scans can identify disturbances in autoregulation by changes in local metabolism, but the technology is not universally available and resolution of anatomic areas is not as sharp as MRI or CT. Electroencephalography (EEG) is useful for identifying subclinical seizure activity exhibited by some TBI patients, and plays a role in brain death determination. The future modalities which may enter the diagnosis and management of TBI include functional MRI and tractography, which may provide prognostic information for patients on the function they can expect to be affected after their injury and to track the progress of recovery.

Prehospital patient assessment

Patients with potential TBI fall into two general categories: low risk and high risk for having an injury that will require neurosurgical management. Low risk patients generally have a Glasgow Coma Scale (GCS) score of 14 or 15, and have no signs or symptoms suggestive of an intracranial injury such as vomiting or severe headache. Further, low risk patients will have normal pupils and no visual complaints, age under 60, and will not be taking anticoagulants (Luerssen et al., 1988; Marshall et al., 1991; Signorini et al., 1999; Davis et al., 2007; McMillian and Rogers, 2009). For these patients, the goal of the prehospital provider is to perform the careful history and physical examination needed to direct transport to an appropriate facility. Patients in the high risk category are those with multiple system trauma or a GCS of 13 or less. In this group, the priorities of the prehospital provider are on appropriate management of life-threatening conditions and a targeted resuscitation.

Primary injury

Skull fractures

The incidence of skull fractures in pediatric head trauma series ranges from 2.1% to 26.6% (Sosin et al., 1996). They are seen in 75% of severe TBI, but in less than 10% of minor head traumas. The majority of fractures are the result of direct impact. Skull fractures are typically described as linear, depressed, or basilar. Linear fractures are by far the most common and account for approximately 75% of all fractures (Figs 62.1–62.3). Depressed skull fractures and skull base fractures are occasionally associated with injury to the underlying dural venous sinuses, resulting in venous EDH or thrombosis (Fig. 62.4). Basilar fractures are present in 6–14% of pediatric trauma patients. In up to 80% of cases, secondary complications may occur, including rhinorrhea, otorrhea, ecchymosis over the mastoid bone (“Battle's sign”), periorbital ecchymosis (“raccoon eyes”), hemotympanum, or seventh-cranial-nerve palsy due to compression. Secondary meningitis is a complication of basilar fractures and occurs in 0.7–5% of cases. Basilar skull fractures extending into the petrous bone may also dislocate the ossicular chain or disrupt the otic labyrinth, leading to permanent hearing loss. Leptomeningeal cyst is a unique pediatric lesion that occurs as a delayed complication in 0.05–1.6% of infants and children with skull fractures (Ersahin et al., 2000). Leptomeningeal cysts may present as a so-called “growing fracture” and occur in children who are younger than 3 years of age (Fig. 62.5) (Aubry et al., 2002; McCrory et al., 2005). They result from a tear in the dura underlying the skull fracture, which allows systolic pulsation of the CSF across the fracture line with progressive meningeal herniation and widening of the skull defect (Ersahin et al., 2000). As mentioned before, skull fractures may only be the tip of the iceberg after TBI. CT may underestimate the degree of brain injury. MRI may reveal the total degree of injury in better detail and should be considered if the neurologic symptoms cannot be explained by the CT findings (Fig. 62.6). In addition, multiplanar 2D and 3D reconstructions of the skull may be helpful to better identify and characterize the complexity and extent of a skull fracture (Fig. 62.2).

Fig. 62.1. Lateral computed tomography (CT), scout view, axial CT images (top row) and axial T2-weighted, fluid-attenuated inversion recovery (FLAIR), and susceptibility-weighted imaging (SWI) images (lower row) of a 2-year-old girl who sustained a linear nondisplaced right frontal skull fracture complicated by an epidural hematoma after a fall. The child presented a week after the fall with progressive headache. The lateral scout view shows the linear fracture (large arrow); due to the fact that the fracture is predominantly in an axial plane it is difficult to recognize on the axial bone CT image (short arrow). A mixed-density subacute epidural hematoma is seen adjacent to the fracture with mild mass effect on the right frontal lobe. The hematoma is mixed T2/FLAIR hyper- and hypointense and appears SWI-hypointense. An additional chronic hematoma is seen subcutaneously.

Fig. 62.2. Axial computed tomography and three-dimensional skull image of a 20-month-old girl with an extensive subdural hematoma along the right cerebral hemisphere, global brain swelling, significant midline shift, subfalcine as well as transtentorial brain herniation, effacement of the basal cisterns, and a right occipital skull fracture extending from the occipital synchondrosis into the adjacent lambdoid suture secondary to a motor vehicle accident with prolonged extraction. Small focal hyperdense shear injuries are noted in the posterior brainstem and left temporal lobe.

Fig. 62.3. (A) Lateral skull, anteroposterior (AP) chest, and AP left foot chest X-rays of a 2-month-old baby boy who “fell from the father's lap while being changed” and subsequently became lethargic with repeated episodes of vomiting. A mildly widened right skull fracture (short arrow) is seen in combination with multiple bilateral, partially healing rib fractures (long arrows) and fractures of at least two metatarsal bones (arrow). Findings are highly suspicious for nonaccidental injury. (B) Sagittal three-dimensional, and sagittal and coronal computed tomography images of the same baby boy confirm the extensive right parietal skull fracture as well as a hyperdense subdural hematoma along the right cerebral hemisphere. (C) Axial T2-weighted and diffusion-weighted imaging (DWI: top row) and axial susceptibility-weighted imaging (SWI: lower row) magnetic resonance imaging (MRI) images of the same child show bilateral SWI-hypointense retinal hemorrhages (arrow), which are not seen on T2-weighted MRI. In addition, extensive bilateral predominantly nonhemorrhagic DWI-hyperintense shear injuries are seen throughout both cerebral hemispheres as well as SWI-hypointense blood along the convexity bilaterally and within the left occipital horn of the lateral ventricle. All findings are compatible with extensive nonaccidental brain injury. (D) Sagittal T2, short tau inversion recovery and T1-weighted MRI of the spine of the same child show a compression fracture of T2 (large arrow), mild amount of blood within the lower spinal canal (arrowhead), and T1-hyperintense blood in the anterior, superior mediastinum (small arrow) secondary to extensive nonaccidental injury.

Fig. 62.4. Axial computed tomography (CT), T2-weighted, diffusion-weighted imaging (DWI), and coronal magnetic resonance (MR)-venography (top row) and axial CT, T2-weighted, DWI, and susceptibility-weighted imaging (SWI: lower row) images of a 10-year-old boy who fell off a moving golf cart and hit his head. He presented to the hospital after 1 day of progressive headache, nausea, and vomiting. A nondisplaced left temporal fracture (short arrow) is seen with complicating T2/DWI-hyperintense (large arrows) left transverse and sigmoid sinus thrombosis, which was confirmed by MR-venography. In addition, a hemorrhagic T2/DWI-hyperintense, SWI-hypointense cortical contusion is seen within the left hemisphere. This cortical contusion is barely visible on CT. An additional small hemorrhage is noted in the trigone of the left lateral ventricle.

Fig. 62.5. (A) Axial computed tomography (CT) images of a 1-month-old baby boy who “fell off the dryer” show a large widened left parietal skull fracture with extensive subdural blood along the left cerebral hemisphere extending into the interhemispheric fissure, subarachnoid blood, as well as a hypodense left temporal/parietal contusion. The imaging findings are not consistent with the trauma history: nonaccidental injury was confirmed. (B) Follow-up sagittal and axial T1-weighted (top row) and axial T2-weighted (lower row) images of the same child show progressive herniation of the injured left parietal lobe through the progressively widened, growing fracture. Significant residual T1-hyperintense subdural blood is noted along the supra- and infratentorial brain. (C) Follow-up coronal skull, three-dimensional CT (top row) and coronal CT images (lower row) show a progressive pseudomeningoencephalocele herniating through the markedly widened skull defect. The left parietal bone is elevated by the cerebrospinal fluid-filled cyst. (D) Follow-up axial T2-weighted magnetic resonance images show a complete resolution of the brain herniation after plastic reconstructive surgery of the skull defect. Significant bilateral, left dominant chronic brain atrophy is seen with enlargement of the ventricles.

Fig. 62.6. Axial computed tomography (CT) and T2-weighted magnetic resonance imaging (MRI) show a subtle subcutaneous bump in the right occipital region (coup) and a small contralateral nonhemorrhagic cortical contusion in the left temporal lobe (contrecoup) in a 12-year-old boy who fell from a top bunk bed. On CT the cortical contusion is barely visible; MRI shows the lesion in much better detail.

Subdural hematoma

SDHs are more frequent in infants and younger children than in adolescents. The cortical veins are more easily torn, the plasticity of the skull is high, and the softness of the unmyelinated brain results in more traction forces to the bridging veins, which facilitates the development of subdural hemorrhages. Unlike in adults, SDH in children are often bilateral, are more common in the interhemispheric fissure and along the cerebellar tentorium, and can be extensive due to the lack of dural adhesions which are usually present in the adult (Figs 62.2 and 62.7) (Poussaint and Moeller, 2002).

Fig. 62.7. Axial and coronal computed tomography images show a moderate-sized hyperdense subdural hematoma along the right cerebral hemisphere with mild midline shift, subfalcine herniation of the ipsilateral lateral ventricle, as well as mild uncal herniation in a 12-year-old boy who hit his head while walking backwards. He was unresponsive for 15 minutes with seizure activity and recovered after acute evacuation of the subdural hematoma. No fracture was seen.