Accidental Head Injuries in Children

Accidental Head Injuries in Children


Brandon G. Gaynor, Garrett K. Zoeller, and John Ragheb


The management of traumatic injuries has been the focus of medical writings since the earliest known medical document—the Edwin Smith Surgical Papyrus.1 This 3,000-year-old papyrus contains the writings of the ancient Egyptian physician Imohotep, in which he details the rational management of 48 medical cases, 27 of which are cases of traumatic injury. Our current medical practice can be traced back to Imohotep’s rational, experienced (“evidence-based”) approach to medicine.


This chapter focuses on accidental head injuries in children, drawing from the literature and the recently updated “Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents—Second Edition.”2 The incidence, mechanisms, and outcomes of accidental traumatic brain injury (TBI) in children are distinct from those in adults and vary with the age of the child. They also vary from those of nonaccidental TBI in children, who likely represent a unique and distinct group and are reviewed in Chapter ▶ 52. In addition, the physiologic and pathophysiologic responses of children to trauma vary with age, and therefore management must be age-specific. A practical approach to the diagnosis and management of accidental traumatic injuries to the developing nervous system is presented in this chapter. Other chapters in the section on trauma deal specifically with such topics as penetrating head injuries, hematomas, critical care management, rehabilitation, and outcomes.


53.1 Epidemiology


Unintentional injuries are the leading cause of death in children. They account for at least a third of deaths in children aged 1 to 14 years and half of those in older adolescents.3 Of all types of traumatic injuries, those to the brain are the most likely to result in death or permanent disability. Among children aged 0 to 14 years, TBI results in an estimated 2,174 deaths annually, 35,135 hospitalizations, and 473,947 emergency department (ED) visits. The annual death rate from traumatic injury in children younger than 4 years is 5 per 100,000. The death rate is higher for children younger than 4 years than for those 5 to 14 years of age. The higher traumatic injury death rate in younger children may sadly reflect the number of inflicted injuries in infants and young children because these figures do not distinguish accidental injury from abusive injury. In adolescents and young adults 15 to 19 years of age, the death rate rises to 19 per 100,000, approaching the rate of death by TBI for young adults.4


The most common mechanisms of pediatric TBI vary by age group. Developmental milestones for movement and ambulation are reflected in the way children are injured. Falls are the leading cause of TBI in children younger than 14 years.5 Children younger than 4 years of age are injured primarily by falls but are also vulnerable to inflicted injuries and motor vehicle crashes. Children 4 to 8 years of age are injured in falls and motor vehicle crashes but also become more at risk for other transportation-related injuries (e.g., bicycles, as pedestrians struck by cars, etc.). The leading cause of death past the age of 14 is motor vehicle crashes, which kill more teenagers than all other causes combined.6,​7


53.2 Types of Accidental Head Injuries


Accidental head injuries in children result in a spectrum of traumatic injuries to the scalp, skull, meninges, and brain that are comparable to those in adults but differ in both pathophysiology and management. The highly vascular scalp is a potential source of major blood loss. Whereas a small loss of blood volume in an adult trauma victim can be trivial, the same blood loss can readily lead to hemorrhagic shock in a newborn, infant, or toddler. This may occur without overt external bleeding in infants and young children. By that token, the presumed plasticity of the brain that is lost with development may provide an outcome advantage for the developing brain compared with its adult counterpart.


Advances in technology impact the delivery of medicine by helping physicians to efficiently evaluate, diagnose, and transfer severely injured patients. Computed tomography (CT) has become widely available and affordable. The luxury of such technology should augment, not substitute for, clinical skills and judgment. It is estimated that for every 700 head CTs ordered, one additional fatal cancer occurs that can be attributed to radiation exposure.8 The judicious use of CT screening and follow-up examinations is important for cost control and patient safety. A recent prospective study of 42,412 children with minor blunt head trauma conducted by the Pediatric Emergency Care Applied Research Network (PECARN) validated a set of predictive rules to identify children who can be observed without CT. Among patients without altered mental status, scalp hematoma, loss of consciousness, severe mechanism of injury, signs of skull fracture, severe headache, or abnormal behavior, fewer than 0.05% had a clinically significant TBI.9 It is likely that a significant portion of CT examinations ordered for children by EDs may not be medically necessary.


The incidence of cervical spine injury in the pediatric population with blunt trauma in the National Emergency X-radiography Utilization Study in Blunt Cervical Trauma (NEXUS) was 1%.10 Although rare, the morbidity and mortality associated with spinal cord injury require accurate and rapid identification of affected patients. The biomechanics of the developing spine also predispose young children to spinal cord injury without radiographic abnormality (SCIWORA).11 The Trauma Association of Canada (TAC) has recently published the first evidenced-based consensus guidelines for clearance of the cervical spine in pediatric trauma patients. These guidelines recommend applying NEXUS criteria with the addition of 45-degree neck rotation in order to clear the cervical spine, reserving CT or magnetic resonance (MR) imaging for those with abnormalities on X-ray and neurologic examination or with neck pain. Validation of these guidelines with prospective data is expected to take several years.12


53.2.1 Injuries to the Developing Skull


The developing skull is thinner, more pliable, and more easily deformed than its mature counterpart. Open sutures provide the skull with some movement and can offset some rise in intracranial pressure (ICP) by expanding the intracranial volume.13 Skull injuries can be classified as nondepressed (linear), depressed, elevated, basilar, or growing.


Linear Skull Fractures


Skull fractures are common injuries in young children. Linear skull fractures are the most common abnormal radiographic findings identified in children after head injury.14 Linear fractures in children may be associated with hemorrhage or significant underlying brain injury, but they usually are not. Complex fractures (i.e., those that are multiple or stellate or that cross a venous sinus) are more likely to be associated with an underlying brain injury or hemorrhage.


Linear fractures represent an injury of sufficient energy that has been dissipated by the skull. The vast majority of linear skull fractures in young children are caused by falls. Anyone who has spent time with toddlers or young children recognizes that falls are extremely common events, even in those younger than 6 months. In a large population-based survey study of 11,466 infants younger than 6 months, there were 3,357 falls in 2,557 children. Despite the large number of falls, of which 53% were from a bed or a piece of furniture, only 21 falls (< 1%), resulted in a concussion or a fracture.15


Linear skull fractures can readily be diagnosed by plain radiography; however, the role of plain radiography in trauma is limited. Clinical criteria should be used to distinguish those patients with risk factors significant enough to warrant computed tomography (CT) from those who can safely be observed without imaging. The importance of a linear fracture is the potential for an associated intracranial pathology.1618 Because of ease of acquisition, availability, relatively low cost, and high sensitivity, CT is the standard test to identify intracranial hemorrhage and fracture in children with significant head injury.19,​20 Occasionally, CT will miss an axially oriented fracture that falls within the plane of the CT scans. Although uncommon, this problem can be avoided by careful inspection of the CT scan scout image.


The vast majority of linear skull fractures require no treatment and heal without sequelae. Children with an isolated, uncomplicated skull fracture and a normal neurologic examination do not require hospital admission. They can be followed at home after a brief period of observation in the ED, provided that the home situation is reliable and caregivers can return promptly in the unlikely event that deterioration occurs. Admission is prudent for patients with persistent vomiting, significant scalp swelling (which can lead to anemia, especially in infants younger than 6 months of age), neurologic deficits, intracranial injury on CT, or suspicion of child abuse.2123


Growing Skull Fractures/Leptomeningeal Cysts


Growing skull fractures, or leptomeningeal cysts, are a rare but well-recognized complication, occurring in approximately 1% of children with skull fractures.24 Skull fractures associated with an underlying dural laceration are the essential substrate of growing skull fractures.25 The growing brain, or perhaps simply the normal pulsations of the brain transmitted through cerebrospinal fluid (CSF), results in herniation of the brain through a dural laceration. Over weeks to months, the edges of the fracture are eroded and/or remodeled, becoming smooth and widening (much as a flowing river erodes its banks). The most common location for growing skull fractures is the parietal region, but they have been described in the orbit and posterior fossa,26 skull base, and anterior fontanel,27 and also as a complication of craniofacial surgery.28 A growing skull fracture presents as a soft, pulsatile mass beneath the scalp, with seizures, or with a progressive neurologic deficit. The diagnosis can be made by skull X-ray in most cases. CT and MR imaging are more sensitive in diagnosing growing skull fractures and can be helpful in identifying the presence of hydrocephalus or an associated porencephalic cyst.29 The treatment of growing skull fractures involves repair of the dura, which invariably requires a dural graft. The dural defect always exceeds the bone defect, which must be taken into consideration when the craniotomy flap is planned. Cranioplasty is also necessary and should be performed with autologous bone whenever possible. A shunt is indicated only when there is associated hydrocephalus, not as a primary treatment for a growing skull fracture. Growing skull fractures should not be allowed to go untreated because the delayed onset of neurologic complications and cranial deformity have been reported.30


Depressed Skull Fractures


Depressed skull fractures are relatively common in children, accounting for approximately 10% of all skull fractures.31 Like linear fractures, most depressed fractures, in which the scalp is intact, do not require surgical intervention. This nonsurgical approach does not appear to increase the risk for seizures or neurologic dysfunction, or to result in greater cosmetic deformity.32 Exceptions may be fractures with a suspected dural laceration or significant underlying brain injury, or fractures in locations of cosmetic importance. A unique subset of depressed fractures in infants and neonates are known as ping-pong fractures. Usually, ping-pong fractures are the result of traumatic deliveries, malpositioned forceps deliveries, or short-distance falls. Most ping-pong fractures involve the parietal bone. When small, these fractures will frequently remodel under the influence of the rapidly growing infant brain without intervention. Although the complication rates are similar for simple depressed skull fractures whether they are treated with observation or surgery, the application of a breast pump or vacuum suction has been reported to be a safe and effective alternative for achieving prompt recovery.33 Larger ping-pong fractures are easily elevated with a small linear incision, a bur hole, and a Penfield elevator, relieving the anxiety many new parents experience while waiting for the deformity to remodel on its own.


Compound or open depressed skull fractures (i.e., those in which the scalp is lacerated) should in most cases be explored, debrided, and repaired. Compound fractures are more often associated with an underlying dural or brain injury and a worse overall prognosis.34 Repair of a compound depressed skull fracture should include a return of the bone fragments to the defect whenever possible. This approach does not appear to increase the risk for postoperative infection and avoids the need for cranioplasty in the future.35 Prophylactic antibiotics beyond the immediate perioperative period, although used frequently in practice, do not appear to reduce the risk for infection.36


A variation of the depressed skull fracture known as an elevated skull fracture has also been described. Elevated skull fractures result from a high-energy impact with a sharp object that elevates the flap by lateral and tangential force vectors or from direct retrieval of a sharp weapon. Once thought to occur only in adults, elevated skull fractures have been reported in children. These unusual fractures are almost always compound and should be managed as a compound depressed fracture with early debridement, reduction, and repair of the underlying dura. Patients with fractures due to a severe mechanism often present with neurologic complications; however, delayed deterioration is also a risk with simple elevated fractures.37,​38


Basilar Skull Fractures


Basilar skull fractures occur in children at approximately the same frequency as in adults, accounting for 15 to 19% of skull fractures.39 CSF leak, via the ear or nose, occurs in about a quarter of the cases and most often stops without intervention. Elevating the head, as well as avoiding straining or any manipulation of the ear or nose, is usually all that is required. In those children (approximately 20%) in whom the leak persists beyond the second or third day after injury, a lumbar drain may be used if not otherwise contraindicated. Prophylactic antibiotics play no role in preventing meningitis in patients with a posttraumatic CSF leak, and their use may actually result in infection by unusual or drug-resistant organisms.4042


Persistent CSF leak after a basilar skull fracture that does not respond to a trial of lumbar drainage requires surgical repair. The presurgical assessment should include MR imaging, which is used to exclude posttraumatic hydrocephalus as well as to visualize the site of the leak. Disruption of the skull base or posterior wall of the frontal sinus and leakage of CSF through a dural defect are readily seen on T2-weighted MR imaging. Thin-section CT is also useful to assess fractures of the skull base and for surgical planning, but it is not a reliable method to identify the site of CSF leak. Radioisotope cisternography with nasal pledgets and CT after contrast cisternography can be used to identify the presence and location of a CSF leak, respectively, but are now rarely needed in the era of MR imaging. Operative repair requires adequate exposure of the fracture site, dural repair, and depending on the size of the fracture defect, a bone graft to support the duraplasty and reconstruct the skull base. Lumbar drainage can be helpful to obtain adequate exposure of the fracture site and to decrease the chance of a persistent CSF leak through the dural repair.


All of the structures of the skull base are potentially at risk after a fracture of the skull base. The carotid artery, venous sinus, cranial nerves, and middle ear structures may be injured, and depending on the location of the fracture, attention should be given to the structures at risk based on the course of the fracture.


53.2.2 Injuries to the Developing Brain


TBIs can be divided into primary and secondary injuries, as well as injuries that are focal or diffuse. Primary TBIs are those injuries that are a direct result of the dissipation of the energy of the traumatic force in the brain. Examples of primary brain injuries are contusion, laceration, hemorrhage, and axonal disruption. Secondary brain injuries result from factors that cause further damage to the brain; these occur as a response to, or result of, the primary traumatic injury and the physiologic derangements that follow. Secondary insults or the contributors to secondary injury are hypoxemia, hypotension, cerebral edema, and elevated ICP.


Traumatic Intraparenchymal Hemorrhage


Traumatic intraparenchymal hemorrhages, also known as brain contusions, are primary brain injuries that result from direct trauma to the brain at the point of impact. Focal contusions may also be the result of impact from an overlying fracture or a deceleration injury as the moving brain strikes the inner table of the skull. The injuries may occur at the point of impact (coup) or opposite the point of impact (contrecoup). Typically, focal contusions occur over the basal frontal or petrous regions and the frontal or temporal poles. The vast majority of focal hemorrhagic contusions do not require surgical intervention unless they are associated with a compound fracture or if they are of sufficient size to require evacuation. Serial CT and close neurologic observation in a monitored setting are required for patients with focal hemorrhagic contusions. A retrospective cohort found that 28.5% of patients with abnormalities on initial CT who underwent repeated examinations within 24 hours had had a radiographic progression. Intraparenchymal, subdural, and epidural hematomas or cerebral edema should be managed as a high risk for deterioration.43


Concussion and Diffuse Axonal Injury


Diffuse injuries to the brain are the result of deceleration or angular acceleration injuries to the head. The spectrum of diffuse brain injury ranges from subclinical concussion to severe diffuse axonal injury. In its mildest form, diffuse brain injury is exemplified by the remarkably common concussion. It has been estimated that 144,000 ED visits for children younger than 19 years have a discharge diagnosis of concussion.44


The hallmark of concussion is a brief (seconds to minutes) loss of consciousness. Although a loss of consciousness is sufficient to diagnose concussion, it is not necessary. CT of the brain is usually normal. There can be a period of confusion or amnesia afterward. Concussion is frequently associated with vomiting in children, which may necessitate admission to the hospital. Efforts have been made to grade the severity of concussion based on the length of loss of consciousness, the presence and duration of amnesia, and errors in mentation.4547 The subtle cognitive, neuropsychological, and physical consequences of concussion are now recognized more often as a result of the development of grading systems, but none of the grading scales has been validated in children. The sequelae are more readily identified after repeated concussions and, not surprisingly, in those who are more thoroughly tested.


Growing public awareness of concussion and perceived “minor” TBIs has been accompanied by a rise in ED visits for sports-related TBIs in the United States. In 2009, there were 248,418 ED visits for sports-related TBIs, an increase of 62% from 2001. Seventy-one percent of patients seen in the ED for recreational or sports-related TBIs are male. Activities associated with the highest incidence of nonfatal TBIs from 2001 to 2009, according to data from the Centers for Disease Control, are bicycling, football, playground activities, basketball, and soccer. However, the number of mild and nonfatal TBIs is likely much higher because these statistics do not account for the many unreported or unrecognized injuries.48


Concern exists regarding the cumulative effects of repeated concussion and the risk for catastrophic “second-impact” types of injury. The long-term sequelae of a single concussion on the developing brain are unknown, although most patients are expected to make a full recovery. Evidence-based guidelines for the management of concussion are lacking, but cognitive and physical rest with a gradual return to activity and careful observation of symptoms are advocated. Children should not return to activities that entail a risk for further injury until their memory, behavior, cognition, and neurologic examination have returned to normal.49,​50 Difficulty arises with young, overachieving athletes and their parents, who insist on putting themselves at risk for further injury by returning to play. There is room for better collaboration among schools, parents, coaches, and physicians to minimize the impact of concussion. Recognition of this fact has resulted in the passage of laws in most states mandating the evaluation of any school-aged athlete suspected of having a concussion and clearance before the athlete may return to play.50


On the continuum of diffuse brain injury, at the opposite end of the spectrum from the simple, uncomplicated concussion is diffuse axonal injury. This is thought to be caused by shearing forces between gray and white matter or within subcortical regions as a result of rotational or angular acceleration and deceleration forces. In the early days of CT, patients with diffuse axonal injury presented in a coma with abnormal posturing. Their CT scans were described as normal or as exhibiting small punctate hemorrhages of the gray–white junction, brainstem, or corpus callosum. Today, the diffuse nature of this type of injury is readily evident on MR imaging, which can reveal widespread punctate areas of signal abnormality or subtle hemorrhage felt to reflect axonal injury.51


Patients with diffuse axonal injury are usually the victims of high-velocity crashes; children with this injury are typically pedestrians or cyclists hit by cars, or passengers in motor vehicles involved in high-speed crashes. In infants and toddlers, these mechanisms may also be associated with craniocervical injuries because of the large size of the head relative to the body, lax spinal ligaments, and relatively weak cervical musculature. Victims of diffuse axonal injury are unresponsive or posturing at presentation and may have cranial nerve signs. ICP monitoring is indicated in those patients with a Glasgow Coma Scale score of 8 or less, although it is usually not elevated in diffuse axonal injury.52,​53 Recovery after diffuse axonal injury is slow, protracted, and usually incomplete. Although not practical in the acute setting, outcomes research on MR abnormalities with techniques like diffusion tensor imaging and functional MR imaging is warranted.


The neurosurgical management of brain injury in children focuses on the preservation of function. Aside from injury prevention, the essence of treatment is the prevention or control of secondary injury to the brain that is precipitated by the initial trauma. The critical care management of TBI is discussed in Chapter ▶ 56. The cornerstone of the neurosurgical management of TBI is ICP control. ICP monitoring in infants and children differs from that in adults in both techniques used and thresholds for intervention. Normal ICP in children is not the same as in adults, and therefore lower ICP thresholds may be used, but it has yet to be studied whether more aggressive treatment thresholds positively affect outcome in children. The guidelines support a Level 3 option of using 20 mm Hg as the cutoff for treatment.2 In infants and toddlers, techniques of ICP monitoring that require placement of a “bolt” or a threaded device secured in the skull may not be feasible. The thin skull of an infant or young child may not provide adequate purchase for the threads of the device to be secured in the skull; however, many widely used devices have alternatives for tunneling. The gold standard technique of ICP monitoring remains placement of a ventriculostomy catheter. External ventricular drains offer both ICP monitoring and the therapeutic option of CSF drainage. Continuous drainage, however, sacrifices real-time ICP monitoring and may be supplemented with a separate ICP monitor or the use of an external ventricular drain that is coupled with a fiberoptic monitor. Infection can be minimized with meticulous technique, diligent nursing care, and the use of an antibiotic-impregnated external ventricular catheter whenever possible.54


Surgical procedures to control medically refractory elevated ICP should be tailored to the individual pathology and maximize cranial volume. Data suggest that decompressive craniectomy reduces ICP and may be useful for treating medically refractory elevations in ICP.55,​56 Current guidelines list decompressive craniectomy with duraplasty as an option for patients with early signs of herniation or medically refractory intracranial hypertension.2,​57 Although the type of procedure that works best is unclear (unilateral vs. bilateral craniectomy, duraplasty vs. no duraplasty), it appears that decompression procedures should be reserved for patients considered salvageable. This may include patients who deteriorate neurologically without a focal mass lesion and who have either unilateral or bilateral hemispheric swelling. This scenario of hemispheric swelling is exacerbated by impaired autoregulation and is not uncommon in infants after nonaccidental trauma.58


53.3 Complications: Seizures


Seizures complicate head injuries in children at least as often as in adults, at a rate of approximately 5 to 12%, although younger children may be more susceptible.59,​60 The incidence may be higher for those with the most severe TBIs.61 The vast majority of seizures after head injury are impact seizures, which occur within the first 24 hours after injury. Early posttraumatic seizures are associated with worse outcomes and greater severity of injury. Some observational studies have found seizure prophylaxis with antiepileptic drugs to be protective for early seizures but not for posttraumatic epilepsy.62


53.4 Conclusion


TBIs are the most common cause of death in young people and therefore represent a significant public health problem and a medical challenge. Concussions, which are now recognized as a brain injury, may have significant cumulative sequelae, and effort should be made to protect the child with a concussion from further injury. The best treatment is prevention. It is hoped that injury awareness education programs like ThinkFirst (www.Thinkfirst.org) and universal seat belt laws and helmet laws for children will reduce cases of TBI in our society. Advances in critical care medicine, cerebral monitoring, and the control of secondary brain injury will offer the greatest potential in the future to limit the consequences of TBIs. Neurosurgical intervention remains the cornerstone of treatment for TBIs, allowing the rapid identification and management of mass lesions, the control of secondary injury, and the monitoring and management of elevated ICP.




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Jul 16, 2016 | Posted by in NEUROSURGERY | Comments Off on Accidental Head Injuries in Children

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