Acquired Brain Injury in Children

CHAPTER 13

ANA C. ALBUJA

ROBERT BAUMANN

OVERVIEW

Acquired brain injury (ABI) is defined as a postneonatal injury to the brain, most commonly as a result from a traumatic brain injury (TBI). Other etiologies include hypoxic–ischemic encephalopathy (HIE), cerebrovascular disease, and infection (van Tol, Gorter, DeMatteo, & Meester-Delver, 2011). Brain injuries that are present before the 28th day of postnatal life are classified as congenital, while those occurring past the 28th day are considered to be acquired. Since TBI, and concussion in particular, is the most common cause of ABI in children, this chapter will be focused on this topic.

HISTORY

The term “concussion” originates from the Latin verb concutere, “to shake violently” (McCrea, Hammeke, Olsen, Leo, & Guskiewicz, 2004). Acute management of TBI with trepanation, both for adults and for children, was already described in the writings of Hippocrates of Cos (c. 460–c. 370 BCE) (Missios, 2007) (see Chapter 1).

PATHOPHYSIOLOGY

TBI causes two injury types: primary and secondary. Primary injury is the mechanical damage that occurs at the time of trauma. It can lead to soft tissue lacerations, skull fractures, and a variety of central nervous system (CNS) lesions such as epidural or subdural hematomas, cerebral contusions, intracerebral hematomas, intraventricular hemorrhage, or diffuse axonal injury (see Chapters 1 and 2).

Immediately after the primary injury, TBI leads to a dysfunctional cascade involving multiple abnormalities in the CNS, which are collectively known as the secondary injury. These include molecular changes such as disruptions in adenosine triphosphate metabolism, release of glutamate, and accumulation of free radicals and intracellular calcium. At the cellular level, injury to the cytoskeleton, loss of cell membrane integrity, and dysfunctional axonal transport are also prominent phenomena. Finally, neuronal metabolism is affected by changes in cerebral blood flow (Rose, Weber, Collen, & Heyer, 2015). If severe enough, the ultimate outcome of the secondary injury may include cerebral infarction, edema, and brain herniation.

Once a primary injury occurs, most therapies aim at decreasing the extent and severity of the secondary injury. The view that children usually have more favorable outcomes after ABI due to greater potential for plasticity is now being challenged. When the developing brain of a child is injured, immature myelination and potential impairments in neuronal plasticity might ensue, increasing the likelihood of functional deficits later in life (Ajao et al., 2012).

ETIOLOGY

The mechanism of injury for pediatric TBI varies with age. In infants and young children, nonaccidental (abusive) TBI is an important etiology of brain injury and is commonly a repetitive insult (Duhaime, Christian, Rorke, & Zimmerman, 1998; Ewing-Cobbs et al., 2000). The incidence of nonaccidental TBI is underreported because only cases that are correctly diagnosed are conveyed in the general statistics (Mulpuri, Slobogean, & Tredwell, 2011). The main causes of accidental TBI in infants and children are falls and being struck by or against objects or other persons (Centers for Disease Control and Prevention [CDC], 2014; Quayle et al., 2014).

In the case of toddlers, falls are the main mechanism of injury. If the history and injury pattern are not consistent, nonaccidental trauma should be considered. When toddlers are involved in motor vehicle–related injuries, they are more frequently struck by a vehicle as pedestrians as opposed to being occupants in motor vehicle accidents.

School-aged children have fewer falls requiring hospitalization as they grow older. In this age group, there is a rise in injuries associated with bicycle crashes. The major causes of TBI in adolescents are assault, sports-related repetitive injury, and motor vehicle accidents (Langlois, Rutland-Brown, & Thomas, 2005; Quayle et al., 2014).

EPIDEMIOLOGY

ABI is a leading cause of death and permanent disability among children and young adults worldwide, with an estimated incidence of 240/100,000 per year (van Tol et al., 2011). TBI is by far the most common cause of ABI in children (Johnson, DeMatt, & Salorio, 2009) and is the most common cause of death in cases of childhood injury. Among all TBI cases, between 88% and 92% correspond to mild injury/concussion (Atabaki, 2013). The rate of emergency room visits is higher for younger children, but hospitalization and death are more frequent among older patients (Wing & James, 2013).

The sport most commonly associated with TBI is football (Atabaki, 2013). There are 1.1 million high school football players in the United States each year, of whom nearly 70,000 are diagnosed with concussion (Broglio et al., 2009). However, this prevalence is likely underreported (Atabaki, 2013; McCrea et al., 2004).

CLINICAL PRESENTATION

As a review from the earlier chapters, the 4th Concussion in Sport Group meeting defined concussion as “a complex pathophysiological process affecting the brain, induced by biomechanical forces” (McCrory et al., 2013). A concussion has to meet four basic requirements: (a) is caused by a direct blow to the head, face, neck, or other region of the body with a force spreading to the head; (b) results in rapid onset of neurological function impairment that lasts for a short period of time and resolves spontaneously; (c) is caused by a functional CNS disruption rather than a structural one; and (d) results in clinical symptoms that may or may not involve loss of consciousness (Echemendia, Giza, & Kutcher, 2015). TBI is a clinical diagnosis, and so history and physical examination are essential. If feasible, information should be obtained directly from the patient. Accurate information provided by witnesses is also very helpful (Atabaki, 2013).

History

Relevant information to be obtained by health care providers includes circumstances of trauma (i.e., falls, motor vehicle accident), height of fall, type of object that caused impact to the head, speed of vehicle, degree of damage to vehicle and injuries to other occupants, whether protective equipment such as seatbelts were used, and so forth (Wing & James, 2013).

Important clinical data to be collected include presence and duration of loss of consciousness, retrograde/anterograde amnesia, confusion, seizures (with as many descriptors as possible), headache, visual changes, nausea, and vomiting (Atabaki, 2013; Field, Collins, Lovell, & Maroon, 2003).

Common signs and symptoms of concussion involve multiple domains:

Physical, such as headache, nausea, vomiting, balance problems, dizziness, problems with vision, sensitivity to lights or sounds, fatigue, numbness, tingling, and confusion

Cognitive, including problems with memory and concentration and feeling mentally foggy and slowed down

Psychological, namely, irritability, sadness, anxiety, and mood swings

Sleep related, such as increased or decreased sleepiness and insomnia (Atabaki, 2013)

Although the aforementioned symptoms usually last 7 to 10 days after the insult, time to recovery may be longer in children and adolescents. Research shows that 80% to 90% of adolescents recover within 2 to 3 weeks after the injury (Covassin, Elbin, & Nakayama, 2010; Field et al., 2003; McCrea et al., 2004).

Be aware that the initial symptoms of a concussion may appear several hours after the trauma, impairing the diagnosis at the time of injury (Echemendia et al., 2015).

Physical Examination

Vital signs should be evaluated and managed accordingly. In particular, look for bradycardia, tachycardia, hypotension, and hypoxia.

TABLE 13.1 PEDIATRIC AND STANDARD GLASGOW COMA SCALE

Table 13.1 depicts the Pediatric and Standard Glasgow Coma Scale, which is used to quantify the severity of acute TBI.

Examine the head, looking for scalp swelling, hematomas, abrasions, and lacerations.

Palpate the scalp looking for obvious fracture or deformity, fontanel fullness in infants, bleeding or drainage from the ears or nose concerning for cerebrospinal fluid leakage.

Also look for signs of fracture of the base of the skull, such as bruising over the mastoid (Battle’s sign) or periorbital bruising (raccoon eyes).

Examine pupils, looking for symmetry, size, and responsiveness.

Perform a funduscopic examination to look for retinal hemorrhages and papilledema (swelling of the optic disc).

Inspect and palpate the cervical spine, looking for potential step-offs or areas of focal tenderness.

There should always be a complete neurological exam.

Changes in the mental status examination should be monitored over time.

The provider should ask the parents if the patient is acting at or close to his or her baseline, especially if the child is younger than 2 years of age (Wing & James, 2013).

DIAGNOSTIC CONSIDERATIONS

The initial evaluation by a health care provider should focus on determining the presence of a life-threatening injury. Emergent evaluation of severe TBI includes evaluation of airway, breathing, circulation, neurological deficits, and other concurrent injuries and is beyond the scope of this chapter (Atabaki, 2013) (see Chapter 2).

Several tools are available for health care providers for the evaluation of concussion. Some of these can be found in the CDC website: (CDC, 2016). The Post-Concussion Symptom Inventory (PCSI)–child/adolescent self-report and parent report forms are developmentally appropriate tools that can aid in the diagnosis and management of concussion (Gioia, Janusz, Isquith, & Vincent, 2008). In order to monitor response to treatment and resolution of symptoms, preinjury scores should be compared with postinjury symptoms. Psychometrically validated concussion-screening tools based on the history and physical examination, such as the Acute Concussion Evaluation (ACE) or the Sport Concussion Assessment Tool (SCAT3), can be used to perform an initial evaluation and diagnosis of patients with concussion (Gioia, Collins, & Isquith, 2008; McCrory et al., 2013).

A single tool or questionnaire is not sufficient for adequate evaluation of the injury. The skilled clinician should use the aforementioned information in the context of the child’s developmental, medical, psychological, and family/school environment to help guide clinical decision making (Gioia, 2015).

Neuropsychological Testing

Baseline neuropsychological testing can be helpful when deciding when a patient should return to play, but it is not mandatory. Although these tests provide clinically significant information, they should not be the sole factor determining the return-to-play decision (Echemendia et al., 2015).

Imaging

The main use of computed tomography (CT) in the acute period after trauma is to rule out life-threatening injuries like skull/facial/spine fractures and the presence of blood products in the brain. CT scans have a significant cost and risks, including a three-fold increase in the risk of developing brain tumors later in life (Pearce et al., 2012).

In 2009, the Pediatric Emergency Care Applied Research Network (PECARN) issued validated prediction rules to identify children at very low risk of clinically important TBI, which is defined as TBI requiring neurosurgical intervention or leading to death (Kuppermann et al., 2009). These criteria allow for a more judicious use of imaging studies and can be found in Table 13.2. If the patient does not meet any of the criteria, the risk of clinically important TBI is very low and imaging is not recommended. Online calculators are also available.

For children younger than 2 years of age, this prediction rule had both a negative predictive value and sensitivity of 100%. For older children, negative predictive value was 99.95% and sensitivity 96.8%. When evaluating the patient days, weeks, or longer after the initial injury, magnetic resonance imaging (MRI) can help detect more subtle abnormalities but does not need to be done routinely (Atabaki, 2013). Functional MRI helps provide information regarding the pathophysiological mechanisms of the injury but is mostly used in research settings (Echemendia et al., 2015).

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