One of the biggest diagnostic dilemmas is when to image a child with the potential for a TBI. Balancing the time, financial costs, radiation exposure, and sometimes legal ramifications versus missing a significant injury weigh on many that treat injured children. Guidelines for when to image patients have been established based on the mechanism of head injury and clinical exam. Many of these guidelines and algorithms were made for adults but were extrapolated to children. The Pediatric Emergency Care Applied Research Network (PECARN) Head CT rules are the most reliable for children. The PECARN rules had 100% sensitivity and negative predictive value for clinically important TBI (ciTBI) in children younger than 2 years old. The negative predictive value and sensitivity for children 2–18 years of age were 99.95% and 96.8%, respectively. As shown, the PECARN rules are effective at ruling out those without significant injuries and do not need a CT scan, but it can also predict pediatric patients with ciTBI (Figs. 16.3 and 16.4 ). The most important factors and first step in determining the need for CT involved the patient’s GCS, presence of altered mentation, and signs of skull fracture (age-dependent). Depending on the age of the patient, other factors came into consideration, as well as the experience of the treating clinician, observation of the patient, and even parental observation. Lastly and most reassuring, PECARN criteria missed less than 0.1% of clinically important TBI in those that did not get a CT, and none required neurosurgical intervention in validation populations.

Adapted from: Identification of children at very low risk of clinically important brain injuries after head trauma: a prospective cohort study. PECARN guidelines for CT imaging in children less than 2 years of age.

Adapted from: Identification of children at very low risk of clinically important brain injuries after head trauma: a prospective cohort study. PECARN guidelines for CT imaging in children 2–18 years of age.

CT is nearly universally used as the initial tool for imaging in the acute phase of traumatic head injuries. MRI is often useful in a delayed fashion for prognostic purposes and structural injuries; due to the availability and time to acquire images, it is of little use in the acute setting. Occasionally, skull x-rays are used to evaluate acute skull fractures. X-rays are also useful in a delayed fashion to assess for late findings of skull fractures in young infants. Unless stated otherwise, and for the purpose of widespread use in acute injury assessment, CT will predominantly be discussed for acute TBI assessment and management.

Skull fractures typically result from a direct force to the head. In younger children and infants, skull fractures can extend over large areas or even be remote from the applied force due to deformational changes of the skull. Evidence of soft-tissue injuries of the scalp overlying skull fractures can be present, including edema, hematoma, laceration, and even radiopaque foreign bodies. Skull fractures are classified as linear, comminuted, depressed, compound, or diastatic. Linear and even comminuted almost always heal without compromise to the structural integrity of the skull (Fig. 16.5 ). Rare exceptions to this are posttraumatic leptomeningeal cysts (“growing skull fracture”), typically occurring in infants less than 1 year old ^, (Fig. 16.6 ). These growing skull fractures occur when there are multiple layers disrupted as the result of the injury (bone, dura, arachnoid, etc.). Brain growth in a young child can drive the separation of the bone edges, but other high-pressure intracranial processes, such as hydrocephalus or venous outflow disruption, can also cause these growing skull fractures to expand. Depressed skull fractures have a higher association with intraaxial brain injuries at the site of the fracture. Surgical elevation of simple depressed skull fractures rarely improves a patient’s neurological status, and surgery is typically reserved for those with cosmetic deformity. On the other hand, depressed skull fractures with overlying scalp laceration (“open, depressed skull fracture”) all require surgical irrigation and debridement of all affected layers to lower the risk of infection (Fig. 16.7 ). Since this requires removing the bone to inspect the dura and brain, correction of the depressed bone is done at the same time.

Comminuted skull fracture ( white arrowheads ) with diastatic fracture of the temporal squamosal suture ( white arrow ).

Same patient as Fig. 16.5. CT with 3D reconstruction. The patient was lost to follow-up for 18 months and returned with a large palpable skull defect consistent with a growing skull fracture ( black arrowheads ).

CT without contrast with 3D reconstruction. Unfortunate patient that was assaulted with a crowbar. (A and B) There are extensive fractures of the frontal, parietal, and temporal bones; also present are bifrontal contusions and an acute SDH. White arrows show the edges of full-thickness skin lacerations. (C) 3D reconstruction showing the extensive fractures more clearly.

The skull base is made up of several bones, including the temporal, occipital (including the clivus), sphenoid, frontal, and ethmoid. Portions of the frontal, sphenoid, and ethmoid bones make up parts of the skull base and the orbit. The complex bony anatomy of the orbit is made up of several other bones, with more extensive discussion in specialized facial and ophthalmological trauma texts. Fractures of the skull base are commonly referred to as basal or basilar skull fractures. Most basal skull fractures involve the temporal bone. These fractures can involve the middle and inner ear structures, including the seventh and eighth cranial nerves. Leakage of cerebrospinal fluid (CSF) is also possible. Clinically, “Battle sign” or ecchymosis of the skin overlying the mastoid is present. Specific CT sequences can readily identify these fractures, and they are also commonly found on regular CT imaging of the head. Fractures of the sphenoid and clivus typically prompt vascular imaging, as the internal carotid arteries and arteries of the posterior circulation may be compromised. The sphenoid bone also houses the pituitary gland, and endocrinopathies can result, the most urgent being diabetes insipidus and cortisol deficiencies. Finally, the classic finding in anterior skull base fractures (Fig. 16.8 ) is “racoon eyes,” referring to periorbital ecchymosis. CSF rhinorrhea can also result from fractures of the anterior cranial base. Both CSF rhinorrhea and otorrhea usually resolve spontaneously with conservative measures, but occasionally temporary CSF diversion is needed; rarely are craniotomy or endonasal procedures required. Although a risk of infection exists, prophylactic antibiotics are not currently recommended with posttraumatic CSF leakage due to skull base fractures. ^,

Axial CT without contrast. Patient with extensive anterior skull base fractures of the frontal, ethmoid, and sphenoid bones ( white arrowheads ) from a falling tree branch. This patient also had open, depressed skull fractures and required repair of these skull base fractures and temporary CSF diversion to prevent CSF leak. The patient has returned to full activities, including playing football.

EDH is classically a biconvex extraaxial hyperdense hematoma adjacent to the skull and brain (Fig. 16.9 ). The epidural space is a “potential” space and an EDH has an associated skull fracture and hematoma associated with arterial bleeding in 85%–95% of cases. Occasionally the hematoma is associated with venous bleeding, and this commonly occurs in the posterior fossa near the dural venous sinuses (Fig. 16.10 ). One other site of venous EDH can be at the vertex, with fractures near the superior sagittal sinus. The other CT imaging feature that distinguishes an EDH from a subdural hematoma (SDH) is that EDHs do not cross suture lines. Much discussion is made of the shape of extraaxial hematomas as they appear on imaging (EDH, SDH), but there are variations of each. Because the dura is so tightly fixed to the suture lines of the skull, EDHs are confined at these fixation points.

Axial CT without contrast showing acute EDH ( white arrowheads ) and right parietal skull fracture ( white arrow ). Note the midline shift of 9 mm ( green lines ). This infant required emergent evacuation of the EDH.

(A and B) Axial and sagittal CT without contrast showing acute EDH due to venous bleeding from the transverse sinus. This hematoma required emergent craniotomy and tamponade of the bleeding venous sinus. (B) The supratentorial and infratentorial extension of the EDH.

The clinical presentation is classically a blunt blow to the head, followed by a lucid interval, and then a sharp decline in neurological status; this is seen in about half of patients. Surgical indications and conservative management guidelines are listed in Table 16.1 . In those that do not require immediate surgical intervention, delayed expansion of EDH can occur in 10%–30% of patients within the first 24–48 hours. ^, Hence, patients conservatively managed need close neuromonitoring, many times in the pediatric intensive care unit, and often require repeat CT to assess for stability of the EDH on imaging. Without another explanation (medications, seizure) nearly all patients rapidly declining in the face of an EDH, regardless of size, require surgical evacuation of the hematoma. Every patient requiring surgery should have a craniotomy to identify the vascular structure causing the hemorrhage. Burr hole drainage is not definitive treatment, as it does not address the source of the arterial bleeding and may be entertained only in emergent situations where craniotomy is unavailable and signs of brain herniation are present.

The subdural space, like its epidural counterpart, is a “potential” space, and any substance in this space is pathological. It is between the dura and the outer layer of the arachnoid, and has bridging veins coursing through, which are the most common source of bleeding. Other sources of bleeding can be from parenchymal injury. There is a higher magnitude of parenchymal damage with ASDHs compared to EDHs; patients with ASDHs typically have more severe brain injuries, poorer exams at presentation, and long-term sequela are more likely. CT imaging typically shows a crescent-shaped, homogeneously hyperdense hematoma along the convexity of the brain. In contrast to EDH, ASDHs can also cross suture lines.

Due to the more extensive primary injury to underlying brain structures (Fig. 16.11 ), surgical considerations must address not only the ASDH, but the underlying brain injury as well. At times this requires placement of intracranial pressure (ICP) monitors and/or not replacing the bone at the time of surgery to allow for posttraumatic swelling. Leaving the bone off (decompressive craniectomy) allows for extracranial swelling of the brain, thereby potentially reducing the secondary injury due to the confining properties of the skull. Defined surgical criteria have been established, but a case-by-case approach is often taken in ASDH treatment (Table 16.2 ). The surgical management of ASDH and chronic subdural hematoma (CSDH; discussed below) differs. ASDH is treated by craniotomy or craniectomy, whereas CSDH can often be treated with burr hole drainage. Due to the solid consistency of acute hematoma in the subdural space, ASDH patients meeting the indications for surgery cannot be temporized with burr holes. Burr holes also do not address the underlying brain injury and swelling.

Axial CT without contrast before (A) and after (B) surgical evacuation of left subdural hematoma ( white arrows ). Note the midline shift ( green lines ). (C) The further extent of injury on axial diffusion-weighted MRI of the underlying cortex ( white arrowheads ), including the caudate of the basal ganglia ( white diamond ).

CSDH in children can occur in many situations, but they are most common with abusive head trauma (AHT), children with thin cortical mantle and cerebrospinal fluid diversion devices (ventriculoperitoneal shunt, endoscopic third ventriculostomy), postoperative craniotomy patients, and those with anticoagulation. Fortunately, children on anticoagulation are rarer than in the adult population, as it is a major risk factor for CSDH in adults. Two of the causes listed are created by neurosurgical intervention, and fortunately, these children are typically followed with serial images. Regardless of the mechanism, CSDHs first start with a traumatic event. Nearly all resolve spontaneously, but some fail to do so as a result of a spiraling pathophysiological mechanism. Breakdown of blood products is mediated by an inflammatory effusion in the subdural space. Rather than reabsorption, these persistent effusions are trapped in the subdural space, which in turn creates more stretch on bridging veins, which in turn causes the vessels to tear or be more easily torn with innocuous trauma. Sometimes, fragile neomembranes also form that are prone to minor traumatic events that further worsen the problem. CSDH can have a long time course since this process can take weeks to months to develop. The size and imaging heterogeneity of CSDH can be quite striking (Fig. 16.12 ). Since the brain has time to accommodate, a large volume and size of fluid can enter the subdural space compared to ASDH. Frequently, a dramatic midline shift is present that would be fatal in acute trauma; radiologic interpretations of these scans can lead to emergent recognition of a chronic problem.

Axial T2-weighted MRI showing a chronic subdural hematoma with at least two compartments (numbered 1 and 2). Membranes ( black arrowheads ) between the compartments are common, and many times a further source of hemorrhage. Note the normal vasculature in the subarachnoid space ( white arrow ).

Guidelines for surgical intervention have not been established for these children, so each case is individualized. Nonsurgical intervention in the adult population, in the form of middle meningeal artery (MMA) embolization, is showing promise as a therapeutic tool, but studies are lacking in children. There are published case reports, but a clinical treatment recommendation is far from established for MMA embolization in children. Burr hole drainage for children that need surgery is the mainstay of treatment. Given the small incision and minimal operative time, burr hole drainage can treat most CSDHs, but craniotomy is needed at times, as are subdural shunt placements.

Intraparenchymal hematomas (IPH or ICH) are referred to as “contusions” or “bruises” of the brain parenchyma. These injuries are common at the site of coup or contrecoup injuries. With time and repeat imaging, it is not uncommon to have expansion of hemorrhage, or development of low-attenuation signal indicating peripheral vasogenic and cytotoxic edema around the original hemorrhage (Fig. 16.13 ). These injuries are also common along the skull base at basal portions of the frontal and temporal regions, in close proximity to bony structures of the skull base. The clinical ramifications of these injuries are dependent on the location, and surgical management is most dependent on the size of the IPH and clinical symptoms (Table 16.3 ).

Axial CT without contrast showing left temporal intraparenchymal hemorrhage ( white arrows ). The initial injury was 24 hours previous to this CT scan, so there is peripheral hypodense signal surrounding the IPH, indicating evolving edema ( white arrowhead ).

It is important to distinguish posttraumatic from spontaneous IPH. IPH in high-energy mechanisms (MVC, fall from a height, known blunt force trauma, etc.) is treated as any traumatic brain injury. However, an unconscious patient without clear evidence of a traumatic event should have nontraumatic mechanisms ruled out. These mechanisms include vascular malformations, which can have devastating consequences if left untreated. Spontaneous loss of consciousness can be a clinical presentation of these lesions, and prompt vascular imaging is required.

Traumatic subarachnoid hemorrhage (tSAH) is in the space between the arachnoid and pia mater which is a normal space containing CSF called the subarachnoid space. tSAH is commonly from injury to small vessels and parenchyma along the surface of the brain. It is common to have associated cortical contusions as well. Hemorrhage can often follow the cortical surface or track into the sulci, including the deeper cisterns and fissures of the brain (Fig. 16.14 ). Clinical presentation is typically not tied to the amount of tSAH, but of other injuries. Isolated tSAH typically presents with mild symptoms and is rarely surgical; many patients do not even require hospital admission.

Axial CT with contrast demonstrates extensive traumatic subarachnoid hemorrhage (tSAH) and air in the basal cisterns ( white arrows ). Subarachnoid blood can also be seen in multiple sulci ( white arrowheads ).