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698 SECTION 12: Pediatrics as expansion of the hematoma causes partial or complete obstruction. Abdominal pain and bilious vomiting are the most common symptoms.86 The seatbelt injury complex is a pattern of blunt abdominal injury seen in children who are inappropriately restrained with a lap belt positioned over the abdomen instead of the pelvic girdle. Acceleration-deceleration forces crush the bowel between the seatbelt and the spine. Classic findings include a “seatbelt sign” (abdominal wall contusion in the distribution of the lap belt), with small bowel injury and Chance fractures of the lumbar spine. Trauma from the lap belt is also associated with injury to the mesentery, renal vasculature, inferior vena cava, aorta, ureters, and solid organs. A seatbelt sign may be present in >15% of children with blunt torso trauma secondary to motor vehicle collisions and, when present, confers a greater than fivefold increased relative risk of intra-abdominal injury requiring intervention. 102 The presence of a Chance fracture is associated with a 50% incidence of associated intra-abdominal injury. PEDIATRIC SPINE AND SPINAL CORD INJURY  PEDIATRIC CERVICAL SPINE TRAUMA Guidelines for immobilization and imaging and information on specific injuries are provided in Chapter 112, “Cervical Spine Injury in Infants and Children. ”  PEDIATRIC THORACIC AND LUMBAR SPINE TRAUMA Children account for only 2% to 5% of all spine injuries, and only 5% of pediatric fractures occur in the spine. 103 Up to 60% of pediatric spine injuries involve the thoracic or lumbar spine, with lumbosacral injuries accounting for two thirds of spinal injury hospitalizations. 104 Pediatric spine injury has a bimodal age distribution, with one peak in children <5 years and another in children >10 years of age. Falls and motor traffic–related injury account for the first peak; motor vehicle collisions account for the majority of spine injuries in older children, although sports-related mechanisms are an important cause of thoracolumbar spine injury in adolescents. 105 Penetrating trauma accounts for <5% of pediatric spine injury, occurs primarily in adolescents, and is associated with greater morbidity than blunt trauma. The pediatric spine differs from that of adults in that children have greater ligamentous elasticity and flexibility, more horizontal facets, wedge-shaped vertebral bodies, and relatively weak musculature, par ticularly before the age of 8, with a transition toward adult anatomy and physiology after this age. Distraction forces can result in Salter-type fractures of the thoracolumbar spine in children, and anatomic differences make multilevel injuries more common in children aged 9 to 16 years in the setting of compression forces. 103,107 Evaluate the pediatric spine during the secondary survey with care ful palpation of the entire spine and paraspinous region for tenderness, step-offs, crepitus, bruising, or open injuries. Physical examination is 87% sensitive and 75% specific for thoracolumbar injuries. Obtain anteroposterior and lateral radiographs of the entire spine in all children with symptoms or signs of spinal injury during physical exam, because up to one third of children with spine injury have two or more spinal fractures. 107 CT scan should be limited to those with neurologic deficits, obvious bony injury on plain film, or significant concern for intra-abdominal or intrathoracic injuries requiring cross-sectional imaging for other reasons.

cal exam, because up to one third of children with spine injury have two or more spinal fractures. 107 CT scan should be limited to those with neurologic deficits, obvious bony injury on plain film, or significant concern for intra-abdominal or intrathoracic injuries requiring cross-sectional imaging for other reasons. Stable children with thoracolumbar spine injury associated with neurologic deficits should be imaged with MRI. Thoracolumbar injuries can be classified using the Thoracolumbar Injury Classification and Severity Score System, which appears to be valid in children as well as adults and can help guide the need for operative management. 108 Generally speaking, clinically stable pediatric fractures without associated neurologic deficits can be treated nonop eratively. Moderate injuries not necessitating surgical decompression or fixation may be considered for bracing depending on age and the extent of injury (e.g., thoracolumbosacral orthosis). Scoliosis can be a sequel to spinal cord injury, particularly among younger children. Compression fractures are the most common fracture in the thoracolumbar spine and are usually stable and managed nonoperatively. Fractures of the spinous or transverse processes are often associated with blunt trauma and carry low risk for associated visceral injury; most of these fractures are managed with analgesics and rest, often without immobilization. The flexion-distraction injury known as the Chance fracture deserves special consideration, given the high rate of concomitant intra-abdominal injury.  PEDIATRIC SPINAL CORD INJURY Pediatric spinal cord injury is uncommon, with an estimated annual incidence of 14 per million population under 18 years. 104 Children under 15 years of age account for only 10% of spinal cord injuries, which are often related to motor vehicle collisions and involve the cervical spine (60% to 80%) far more commonly than the thoracolumbar spine. Overall, neurologic recovery is better among children than adults with traumatic spinal cord injury, with incomplete injuries associated with better outcomes. Spinal cord injury without radiographic abnormality, a unique pediatric entity, is far more common in the thoracic spine than the lumbar spine. 107 Spinal cord injuries are frequently associated with other injuries, with rates ranging from 40% to 60%, and most commonly involve the torso, extremities, and cranium. The clinical evaluation and presentation of spinal cord injury and syndromes as well as the principles of physical examination and stabiliza tion are similar to those of adults (see Chapter 258, “Spine Trauma”). As with adults, flaccid paralysis with hypotension and relative bradycardia suggests neurogenic shock; early administration of vasopressors is rec ommended, as aggressive fluid administration can worsen spinal cord edema. Corticosteroids are not recommended to treat acute spinal cord injury in children. Steroids increase the risk of infection and do not result in significant neurologic improvements in children . TRAUMATIC ARREST Emergency thoracotomy has no role in blunt traumatic arrest in children.110 As in adults, the resuscitation of children with blunt traumatic arrest should focus on addressing reversible causes, with deemphasis on CPR and vasoactive agents. Key interventions include (1) obtaining a defini tive airway, (2) managing major external bleeding, (3) chest decom pression and assessment for cardiac tamponade, and (4) administering blood. If there is no return of circulation after these steps, the child is unlikely to survive, and a prolonged resuscitation is futile. ED thora cotomy should be considered for children with penetrating chest injuries who lose vital signs during transport or in the trauma bay, especially if there are signs of life.

g blood. If there is no return of circulation after these steps, the child is unlikely to survive, and a prolonged resuscitation is futile. ED thora cotomy should be considered for children with penetrating chest injuries who lose vital signs during transport or in the trauma bay, especially if there are signs of life. Keep in mind, emergency thoracotomy poses substantial risk of injury to staff. 110,111 REFERENCES The complete reference list is available online at www.TintinalliEM.com. Minor Head Injury and Concussion in Children Paul M.A. Korn Franz Babl INTRODUCTION AND EPIDEMIOLOGY Head trauma is an important cause of morbidity and mortality in children. Over 750,000 children and adolescents with head injuries present annually to EDs in the United States, double that of a decade ago. The highest incidence is in the 0- to 4-year age group. 1 Annual estimates of pediatric sports-related concussion in the United States range from 1.1 to 1.9 million. 2 Although the majority of concussions are not seen in CHAPTER Tintinalli_Sec12_p0669-0996.indd 698 8/2/19 7:49 PM

ed States, double that of a decade ago. The highest incidence is in the 0- to 4-year age group. 1 Annual estimates of pediatric sports-related concussion in the United States range from 1.1 to 1.9 million. 2 Although the majority of concussions are not seen in CHAPTER Tintinalli_Sec12_p0669-0996.indd 698 8/2/19 7:49 PM CHAPTER 111: Minor Head Injury and Concussion in Children 699 HISTORY Obtain a comprehensive history including mechanism and severity of injury and eyewitness accounts. Concussions should be considered in the presence of one or more physical, cognitive, emotional, or sleep changes (Table 111-2). Inquire about loss of consciousness, disorientation, confusion, blank stare, poor balance, gait instability, and posttraumatic seizure. Deter mine if there has been improvement or deterioration since the time of injury, particularly relating to level of consciousness, headache, and vomiting. Gather information relating to previous concussions, preexisting neurologic disorders including migraine, emotional dysregulation, learning difficulties, attention-deficit/hyperactivity disorder, behavioral disorders, and coagulation disorders. Inquire about antegrade and ret rograde amnesia, short-term memory loss, and ability to concentrate. If patients present to the ED beyond the acute stage, determine when the injury occurred; if there has been repeat head trauma, change in mood, change in sleep pattern, or symptom triggers; and if school or physical activity has worsened symptoms. Symptoms of concussion are often nonspecific and may mimic other conditions such as anxiety and depression. Moreover, some individuals may overreport symptoms (reporting resolved symptoms as unresolved, exaggerating the extent and severity of symptoms, fabricating symp toms), whereas others may underreport symptoms. Everyday somatic complaints, such as headache, fatigue, and sleep difficulties, may be misattributed to a head injury. PHYSICAL EXAMINATION Obtain vital signs and perform a general examination to determine extent of all injuries. Look for external signs of trauma including facial TABLE 111-1 Modified Glasgow Coma Scale for Infants and Children Component Infant Child/Adult Score Eye opening Spontaneous To speech To pain only No response Spontaneous To speech To pain only No response Best verbal response Coos and babbles Irritable cries Cries to pain Moans to pain No response Oriented, appropriate Confused Inappropriate words Incomprehensible sounds No response Best motor response Moves spontaneously/ purposefully Withdraws to touch Withdraws to pain Abnormal flexion posture to pain Abnormal extension posture to pain No response Obeys commands Localizes painful stimulus Withdraws to pain Abnormal flexion posture to pain Abnormal extension posture to pain No response

response Best motor response Moves spontaneously/ purposefully Withdraws to touch Withdraws to pain Abnormal flexion posture to pain Abnormal extension posture to pain No response Obeys commands Localizes painful stimulus Withdraws to pain Abnormal flexion posture to pain Abnormal extension posture to pain No response TABLE 111-2 Symptoms of Concussion Domain Symptoms Physical Headache, nausea, vomiting, confusion, dizziness, balance problems, visual changes, fatigue, photophobia, phonophobia Cognitive Fogginess of thought, difficulty with concentration, difficulty with memory, forgetfulness, repeating questions, answering questions slowly Emotional Irritability, sadness, anxiety, emotional lability Sleep Drowsiness, sleeping more than usual, sleeping less than usual, trouble falling asleep, trouble staying asleep healthcare settings, an estimated 378,000 patients were seen as outpatient visits, 150,000 presented to the ED, and 5000 were admitted to hospitals annually in the United States alone. Concussion, minor head injury, and mild traumatic brain injury his torically have had different definitions in medical literature. Typically, minor head injury is defined by Glasgow Coma Scale (GCS) score of 14 or 15 at the time of presentation to the ED. At a major conference of concussion specialists in Berlin in 2016, a consensus definition of concussion was derived: traumatic brain injury induced by biomechanical forces. Concussion may be caused by a direct blow to the head, face, neck, or elsewhere on the body, with an impulsive force transmitted to the head. It typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously. However, in some cases, signs and symptoms evolve over a number of minutes to hours. PATHOPHYSIOLOGY Concussion may result in neuropathologic changes, but the acute clinical signs and symptoms reflect a functional disturbance rather than gross structural injury, and as such, no abnormality is seen on standard structural neuroimaging studies. Blunt head trauma in children often causes diffuse rather than focal injuries. A relatively larger calvarium and weaker cervical musculature in children impair protective mechanisms. The brain rotates around its center of gravity, resulting in diffuse axonal injury and possible subdural hemorrhage. Acceleration and deceleration forces initiate a neurochemical cascade that results in neuronal membrane disruption and axonal stretching. The acute phase of injury is characterized by an increase in cerebral cellular energy demand coupled with insufficient energy substrate delivery resulting in a metabolic crisis. This metabolic mismatch leads to altera tions in neuronal depolarization, ion transport, glycolysis, mitochondrial function, and neurotransmitter release. Global and regional cerebral blood flow is reduced. Stretching of axons due to mechanical forces results in indiscriminate release of neurotransmitters and calcium influx and potassium efflux, resulting in widespread depolarization. Cells respond by activating ion pumps in an attempt to restore the normal membrane potential, which accelerates glycolysis and contributes to a state of hypermetabolism. Intracellular magnesium levels appear to diminish and may remain suppressed for several days. Magnesium is essential for generation of adenosine triphosphate, initiation of protein synthesis, and maintenance of cellular membrane potential. High intracellular calcium levels combined with stretch injury can cause destruction of microtubules within axons. The effect of this disruption leads to axonal swelling and detachment.

s essential for generation of adenosine triphosphate, initiation of protein synthesis, and maintenance of cellular membrane potential. High intracellular calcium levels combined with stretch injury can cause destruction of microtubules within axons. The effect of this disruption leads to axonal swelling and detachment. Most cells, however, appear to recover normal cellular function, so the concussed brain undergoes dynamic restoration and brain function returns to the preconcussed state in the majority of children and youth. In some cases, however, brain structure and physiology may undergo reorganization and long-term pathologic changes. CLINICAL FEATURES The signs and symptoms of concussion are numerous and highly vari able and can develop over seconds to several days following an injury. Children and adolescents may not be fully aware of their symptoms and may not be able to articulate or describe the effects clearly. In infants and very young children, symptoms of neurologic injury may be subtle. Lethargy, irritability, poor muscle tone, breathing abnormalities, and poor feeding should raise concerns of a significant head injury. The GCS is often used as an initial reliable tool for determining severity of brain injury (Table 111-1). Children presenting with a GCS of ≤14 are at increased risk for intracranial injuries. Red flags for serious injury include neck pain or tenderness, double vision, weakness or tingling in the arms or legs, severe or increasing headache, seizure, loss of consciousness, deteriorating mental status, persistent vomiting, and increasing restlessness. A history of a coagulopathy, previous neurosurgery (e.g., shunt), dangerous mechanism of injury (see Table 111-3), and multiple injuries deserve special consideration. Tintinalli_Sec12_p0669-0996.indd 699 8/2/19 7:49 PM

oss of consciousness, deteriorating mental status, persistent vomiting, and increasing restlessness. A history of a coagulopathy, previous neurosurgery (e.g., shunt), dangerous mechanism of injury (see Table 111-3), and multiple injuries deserve special consideration. Tintinalli_Sec12_p0669-0996.indd 699 8/2/19 7:49 PM 700 SECTION 12: Pediatrics and scalp bruising, boggy scalp hematoma, evidence of an open or depressed skull fracture, hemotympanum, “racoon eyes, ” “battle sign, ” otorrhea, and rhinorrhea of cerebrospinal fluid. Scalp hematomas that are large and nonfrontal in location have a higher association with skull fracture in infants <3 months of age, although they are rarely associated with clinically important intracranial injury in otherwise asymptomatic infants and older children. 9,10 Specific bruising and injury patterns in infants and young children raise concern for abusive trauma (see Chapter 150, “Child Abuse and Neglect”). 11,12 Determine the GCS (Table 111-1). Assess orientation and memory for events directly preceding the head injury. Test immediate memory, delayed memory, and concentration. Perform a detailed neck exam, assessing for central spine tenderness, painful or reduced cervical spine range of motion, and focal neurologic deficits. If concerned, the cervical spine should be immobilized until the extent of injury is determined (see Chapter 112, “Cervical Spine Injury in Infants and Children”). Perform a focused neurologic exam including cranial nerve, cerebel lar, motor, sensory, balance, and gait assessment. Assess vestibular-ocular reflexes for gaze stabilization, gaze shifting, and vergence. Damage to any of these systems can lead to complex symptoms that exacerbate and complicate recovery, including balance disturbance, eye tracking dif ficulties, nausea, dizziness, headache, difficulty reading, and difficulty walking. Test visual acuity, extraocular motility, pupillary response to light, and fundoscopy. IMAGING After initial assessment and stabilization, the most immediate question in children presenting with head injuries to the ED is whether they require neuroimaging. Currently, there are no recommendations for electroencephalogram, advanced neuroimaging, genetic testing, and serum biomarkers in the ED setting. Noncontrast head CT identifies and excludes critical intracranial injuries that require immediate or urgent intervention, can be conducted within seconds, and usually does not require sedation. 13,14 Although the need for sedation is increased in agitated or combative children or those <2 years old, the majority can be imaged without sedation by using parental presence. The primary drawback of CT, however, is radiation exposure, which may increase the lifetime risk of brain and other can cers, particularly in young children. 15-17 Although MRI is a radiationfree alternative, it is impractical at this time in the ED due to the time required for imaging. It is generally agreed that children with GCS score of <13 should undergo neuroimaging based on the increased risk of significant intracranial injury. For milder head injuries (GCS score of 13 to 15), multiple clinical decision rules have been developed to assist clinicians in identifying children at increased risk of intracranial injury, help bal ance the risk of missing a significant injury, and minimize the risk of radiation-induced cancer. Decision rules for head injuries use elements of injury mechanism, patient history, and physical examination to riskstratify patients. Although many rules appear superficially similar, they differ in details, inclusion and exclusion criteria (e.g., age limits, injury severity), predictor variables, and the outcomes used ( Table 111-3).

r head injuries use elements of injury mechanism, patient history, and physical examination to riskstratify patients. Although many rules appear superficially similar, they differ in details, inclusion and exclusion criteria (e.g., age limits, injury severity), predictor variables, and the outcomes used ( Table 111-3). The highest-quality, prospectively derived, and externally validated decision rules 18-21 are (1) the prediction rule for the identification of children at very low risk of clinically important traumatic brain injury developed by the Pediatric Emergency Care Applied Research Network (PECARN, United States), 22 (2) the Canadian Assessment of Tomography for Childhood Head Injury (CATCH, Canada) rule, 23 (3) the Children’s Head Injury Algorithm for the Prediction of Impor tant Clinical Events (CHALICE, United Kingdom), 24 and (4) the National Emergency X-Radiography Utilization Study II (NEXUS II, United States). 25,26 These rules were derived based on large numbers of patients in different countries and were based on different baseline imaging rates, ranging from 3% (CHALICE) to 53% (CATCH) for the population under investigation. Whereas PECARN, CATCH, and CHALICE were specifically designed for pediatric head injuries, the premise of NEXUS II was to create a risk decision instrument for headinjured patients of all ages, because the majority of children are seen in mixed EDs that care for both adult and pediatric patients. The main difference between PECARN and the other three rules is that its goal is to identify patients at very low risk of intracranial injury who do not need a CT scan (all predictor variables negative, no CT required), with separate rules for children <2 years and ≥2 years old, whereas the other rules seek to identify the patients who do require a CT scan (any predictor variables positive, CT required). The rules were also designed for patients of different injury severity, with CHALICE designed for all severities (GCS 3 to 15), PECARN for patients with GCS of 14 and 15, and CATCH for patients with GCS of 13 to 15 and with symptoms of mild head injury (blunt trauma to the head result ing in witnessed loss of consciousness, definite amnesia, witnessed disorientation, persistent vomiting, and persistent irritability in the ED [in children <2 years old]). NEXUS II was designed for patients of all severities who had already been selected for CT scans. 25-27 Although all four rules had very high sensitivities when using the rule-specific design and outcomes (PECARN <2 years, 98.6%; PECARN ≥2 years, 96.7%; CHALICE, 98.6%; CATCH, 100%; NEXUS II in children <18 years old, 98.6%; with specificities of 53.7%, 58.5%, 86.9%, 70.2%, and 15.1%, respectively), the accuracy of the rules is difficult to compare due to the many differences in their design. Recently a large external cohort of 20,137 head-injured children was used to compare the pediatric-specific rules using a common outcome (clini cally important traumatic brain injuries, which are defined as death from traumatic brain injury, neurosurgical intervention for traumatic brain injury, intubation of >24 hours for traumatic brain injury, or hospital admission of ≥2 nights for traumatic brain injury in associa tion with traumatic brain injury on CT) in patients with GCS of 13 to 15. 21 All three pediatric rules had high sensitivities (PECARN, 100% [<2 years] and 99.2% [≥2 years]; CHALICE, 92.5%; CATCH, 91.9%) and overlapping confidence intervals, with PECARN <2 years and ≥2 years missing 0 and 1 injured patient, respectively; CHALICE missing 12 patients; and CATCH missing 13 patients. Sensitivities in detecting traumatic brain injury on CT and identifying patients requiring neuro surgery were similar to the detection of clinically important traumatic brain injuries.

PECARN <2 years and ≥2 years missing 0 and 1 injured patient, respectively; CHALICE missing 12 patients; and CATCH missing 13 patients. Sensitivities in detecting traumatic brain injury on CT and identifying patients requiring neuro surgery were similar to the detection of clinically important traumatic brain injuries. As a widely used and highly accurate decision rule, PECARN is pre sented in more detail. The PECARN rule provides guidance for children <2 years and ≥2 years of age (Figure 111-1). 24 The main difference between older and younger rule is the inclusion of vomiting and severe headache as a predictor variable in children ≥2 years and the inclusion of occipital, parietal, or temporal scalp hematomas or palpable skull fractures and the exclusion of vomiting as predictor variables in children <2 years. If all six predictor variables are negative, the risk of a clinically important traumatic brain injury is so low that a CT scan is not necessary. The PECARN group also provides guidance for patients with one or more positive predictor variables (Figure 111-1). Children with higher risk predictor variables— GCS of 14 or other signs of altered mental status, palpable skull fracture (<2 years), or signs of basilar skull fracture (≥2 years)—are at increased risk of clinically important traumatic brain injury and should undergo a CT scan. Children with any of the other four predictor variables are at intermediate risk of intracranial injury, and other factors should be used, such as multiple findings, worsening symptoms, and clinician and parental preferences. TREATMENT The ED management of serious brain injuries is covered in Chapters 110, “Pediatric Trauma” and 250, “Skin Disorders: Face and Scalp” , whereas associated cervical spine injury management is discussed in Chapter 112 and abusive head injuries are discussed in Chapter 150. Once these major injuries have been ruled out, the ED management of concussion focuses on relief of acute or persistent symptoms, patient and family education, and appropriate outpatient follow-up. Strategies for the ED management of specific symptoms related to mild traumatic brain injury and education of patients regarding postdischarge care are discussed below.  HEADACHE Headache is the most common complaint following mild traumatic brain injury, with an onset within 7 days of the initial injury, and can be acute or persistent in nature. Although classified as a secondary Tintinalli_Sec12_p0669-0996.indd 700 8/2/19 7:49 PM

ts regarding postdischarge care are discussed below.  HEADACHE Headache is the most common complaint following mild traumatic brain injury, with an onset within 7 days of the initial injury, and can be acute or persistent in nature. Although classified as a secondary Tintinalli_Sec12_p0669-0996.indd 700 8/2/19 7:49 PM CHAPTER 111: Minor Head Injury and Concussion in Children 701 TABLE 111-3 Predictor Variables and Outcome Measures of PECARN, CATCH, CHALICE, and NEXUS II Clinical Decision Rules 22-25 PECARN <2 y PECARN ≥2 y CATCH CHALICE NEXUS II Primary outcome Clinically important traumatic brain injury; defined as death from traumatic brain injury, neurosurgical intervention for traumatic brain injury (intracranial pressure monitoring, elevation of depressed skull fracture, ventriculostomy, hematoma evacuation, lobectomy, tissue debridement, dura repair, other), intubation of >24 h for traumatic brain injury or hospital admission of 2 nights or more for traumatic brain injury * in association with traumatic brain injury on CT† Need for neurologic intervention; defined as either death within 7 d secondary to the head injury or need for any of the following procedures within 7 days: craniotomy, elevation of skull fracture, monitoring of intracranial pressure, insertion of endotracheal tube for the management of head injury Clinically significant intracranial injury; defined as death as a result of head injury, requirement for neurosurgical intervention, or marked abnormality on CT (defined as any new, acute, traumatic intracranial pathology as reported by consultant radiologist, including intracranial hematomas of any size, cerebral contusion, diffuse cerebral edema, and depressed skull fractures) Clinically important intracranial injuries; defined as substantial epidural or subdural hematoma (>1.0 cm in width or causing mass effect); substantial cerebral contusion (>1.0 cm in diameter or >1 site); extensive subarachnoid hemorrhage; mass effect or sulcal effacement; signs of herniation; basal cistern compression or midline shift; hemorrhage in the posterior fossa; intraventricular hemorrhage; bilateral hemorrhage of any type; depressed or diastatic skull fracture; pneumocephalus; diffuse cerebral edema; diffuse axonal injury Predictor variable ‡§ Mechanism Severe mechanism of injury (MVC with patient ejection, death of another passenger, or rollover; pedestrian/ bicyclist without helmet struck by motorized vehicle; falls >0.9 m; head struck by high-impact object) Severe mechanism of injury (MVC with patient ejection, death of another passenger, or rollover; pedestrian/ bicyclist without helmet struck by motorized vehicle; falls >1.5 m; head struck by high-impact object) Dangerous mechanism of injury (e.g., MVC; fall from elevation ≥3 ft (≥91 cm) or 5 stairs; fall from bicycle with no helmet) High-speed RTA as pedestrian, cyclist, occupant (defined as accident with speed >40 mph or 64 km/h) Fall >3 m in height High-speed injury from projectile or object Persistent vomiting Altered level of alertness, abnormal behavior Coagulopathy History LOC ≥5 s Not acting normally per parent Any or suspected LOC History of vomiting Severe headache History of worsening headache ¶ Witnessed LOC >5 min ≥3 vomits after head injury (discrete episodes) Amnesia (antegrade/retrograde >5 min) Suspicion of NAI (NAI defined as any suspicion of NAI by the examining doctor) Seizure in patient with no history of epilepsy

ny or suspected LOC History of vomiting Severe headache History of worsening headache ¶ Witnessed LOC >5 min ≥3 vomits after head injury (discrete episodes) Amnesia (antegrade/retrograde >5 min) Suspicion of NAI (NAI defined as any suspicion of NAI by the examining doctor) Seizure in patient with no history of epilepsy Examination GCS <15 Other signs of altered mental status (agitation, somnolence, repetitive questioning, slow response to verbal communication) Palpable or unclear skull fracture Occipital, parietal, or temporal scalp hematoma GCS <15 Other signs of altered mental status (agitation, somnolence, repetitive questioning, slow response to verbal communication) Clinical signs of basilar skull fracture GCS <15 at 2 h after injury ¶ Irritability on examination¶ Any sign of basal skull fracture (e.g., hemotympanum, “racoon” eyes, otorrhea or rhinorrhea of the cerebrospinal fluid, Battle’s sign) Large, boggy scalp hematoma GCS <14, or <15 if <1 y old Abnormal drowsiness (in excess of that expected by examining doctor) Focal neurologic deficit Signs of basal skull fracture (hemotympanum, racoon eyes, otorrhea or rhinorrhea of cerebrospinal fluid, Battle’s sign) Suspicion of penetrating or depressed skull injury, or tense fontanelle Neurologic deficit Abnormal behavior Evidence of significant skull fracture Presence of scalp hematoma Note: Although the predictor variables are reproduced verbatim, the order in which the variables from each clinical decision rule are presented has been altered to facilitate comparison. Abbreviations: CATCH = Canadian Assessment of Tomography for Childhood Head Injury; CHALICE = Children’s Head Injury Algorithm for the Prediction of Important Clinical Events; GCS = Glasgow Coma Scale; LOC = loss of consciousness; MVC = motor vehicle crash; NAI = nonaccidental injury; NEXUS II = National Emergency X-Radiography Utilization Study II; PECARN = Pediatric Emergency Care Applied Research Network; RTA = road traffic accident. *Hospital admission for traumatic brain injury defined by admission for persistent neurologic symptoms or signs such as persistent alteration in mental status, recurrent emesis due to head injury, persistent severe headache, or ongoing seizure management. †Traumatic brain injury on CT is defined by any of the following descriptions: intracranial hemorrhage or contusion, cerebral edema, traumatic infarction, diffuse axonal injury, shearing injury, sigmoid sinus throm bosis, midline shift of intracranial contents or signs of brain herniation, diastasis of the skull, pneumocephalus, or skull fracture depressed by at least the width of the table of the skull. ‡In each of the four clinical decision rules, the absence of all of the above predictor variables indicates that cranial CT scan is unnecessary. §NEXUS II predictor variable includes the criterion age >65 years (which is not relevant in pediatric patients). ¶High-risk predictors for CATCH (need for neurologic intervention). Tintinalli_Sec12_p0669-0996.indd 701 8/2/19 7:49 PM

of all of the above predictor variables indicates that cranial CT scan is unnecessary. §NEXUS II predictor variable includes the criterion age >65 years (which is not relevant in pediatric patients). ¶High-risk predictors for CATCH (need for neurologic intervention). Tintinalli_Sec12_p0669-0996.indd 701 8/2/19 7:49 PM 702 SECTION 12: Pediatrics headache (see Chapter 139, “Headache in Children”), posttraumatic headaches often have characteristics of one of the primary headache disorders (Table 111-4), and a history of primary headache disorder may predispose to persistent symptoms after injury. Treat posttrau matic headaches based on the primary headache disorder they most resemble. Determining appropriate pharmacotherapy in the ED is challenging because there is limited evidence for effective treatment strategies. Acetaminophen and NSAIDs (ibuprofen and naproxen) may provide acute relief. Do not provide NSAIDs until intracranial hemorrhage is excluded. After the first few days, NSAIDS may lose their effectiveness. The frequent and prolonged use of over-the-counter analgesics may result in worsening and rebound headaches. Although one previous study suggested hypertonic saline for symp tomatic treatment of acute concussive symptoms,30 the 2018 Centers for Disease Control and Prevention guideline on the diagnosis and management of mild traumatic brain injury among children does not recom mend hypertonic saline outside of the research setting at this time. 31 13.9% of population 4.4% risk of ciTBI Yes CT recommended Yes 32.6% of population 0.9% risk of ciTBI Observation versus CT on the basis of other clinical factors including: • Physician experience • Multiple versus isolated § findings • Worsening symptoms or signs after emergency department observation • Age <3 months • Parental preference CT not recommended ¶ 53.5% of population <0.02% risk of ciTBI 14.0% of population 4.3% risk of ciTBI Yes CT recommended GCS=14 or other signs of altered mental status†, or palpable skull fracture Occipital or parietal or temporal scalp haematoma, or history of LOC ≥5 s, or severe mechanism of injury ‡, or not acting normally per parent GCS=14 or other signs of altered mental status†, or signs of basilar skull fracture History of LOC, or history of vomiting, or severe mechanism of injury ‡, or severe headache Yes 27.7% of population 0.9% risk of ciTBI Observation versus CT on the basis of other clinical factors including: • Physician experience • Multiple versus isolated § findings • Worsening symptoms or signs after emergency department observation • Parental preference CT not recommended ¶ 58.3% of population <0.05% risk of ciTBI FIGURE 111-1. Suggested CT algorithm for children <2 years old (A) and ≥2 years old ( B) with Glasgow Coma Scale (GCS) scores of 14 and 15 after head trauma. ciTBI = clinically important traumatic brain injury; LOC = loss of consciousness. †Other signs of altered mental status include agitation, somnolence, repetitive questioning, or slow response to verbal communication. ‡Severe mechanism of injury includes motor vehicle crash with patient ejection, death of another passenger, or rollover; pedestrian or bicyclist without a helmet struck by a motorized vehicle; falls of >0.9 m (3 ft) or >1.5 m (5 ft) for panel B; or head struck by a high impact object. ∫Patient with certain isolated findings (i.e., with no other findings suggestive of traumatic brain injury) such as isolated LOC, isolated headache, isolated vomiting, and certain types of isolated scalp hematoma in infants >3 months old have a risk of ciTBI substantially lower than 1%. ¶Risk of ciTBI exceedingly low, generally lower than risk of CT-induced malignancies. Therefore, CT scans are not indicated for most patients in this group.

LOC, isolated headache, isolated vomiting, and certain types of isolated scalp hematoma in infants >3 months old have a risk of ciTBI substantially lower than 1%. ¶Risk of ciTBI exceedingly low, generally lower than risk of CT-induced malignancies. Therefore, CT scans are not indicated for most patients in this group. [Reproduced with permission from Kuppermann N, Holmes JF, Dayan PS, et al: Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet 2009 Oct 3;374(9696):1160-1170. Copyright Elsevier.] TABLE 111-4 Posttraumatic Headache Symptoms Resembling Primary Headache Disorders Symptoms Corresponding Primary Headache Disorder Bilateral, moderate severity, dull pressure/squeezing sensation. Location is variable. Triggers are stress, reading, sustained poor posture. Tension type Unilateral, severe, pulsating, associated nausea, vomiting, photophobia, sensory and visual changes. Location may vary. Triggers can be exercise, lights, and sounds. Migraine Unilateral, severe, throbbing, autonomic activation, lacrimation, and rhinorrhea. Pain is often described as retro-orbital or periorbital. Cluster Unilateral, mild to severe in quality, often described as aching. Location is focal, involving the neck. Triggers are neck movement. There is often a history of whiplash. Cervicogenic Tintinalli_Sec12_p0669-0996.indd 702 8/2/19 7:49 PM

on, and rhinorrhea. Pain is often described as retro-orbital or periorbital. Cluster Unilateral, mild to severe in quality, often described as aching. Location is focal, involving the neck. Triggers are neck movement. There is often a history of whiplash. Cervicogenic Tintinalli_Sec12_p0669-0996.indd 702 8/2/19 7:49 PM CHAPTER 111: Minor Head Injury and Concussion in Children 703 Children and adolescents with complex, depressed, or basilar skull fractures should be managed in conjunction with neurosurgery and typically require admission. Stable asymptomatic infants and children with linear, nondisplaced skull fractures with no evidence of intracranial injury are safe for discharge with primary care follow-up.  FOLLOW-UP CONSIDERATIONS The majority of children and adolescents who sustain a concussion will recover within 2 to 4 weeks. The strongest and most consistent predictor of slower recovery is the severity of symptoms during the first few days following injury. A low level of symptoms in the first day following an injury is a favorable prognostic indicator. Approximately one third of concussed children and adolescents, however, will go on to experience ongoing somatic, cognitive, psychological, or behavioral symptoms, commonly referred to as persistent postconcussion symptoms. These symptoms do not reflect a single pathophysiologic entity, but describe a constellation of nonspecific posttraumatic symptoms that may be linked to coexisting or confounding factors (e.g., previous concussions, mental health problems, migraine history, previous neurologic disorders, lack of social supports, female gender, higher level of symptoms, presence of life stressors, substance abuse). They do not necessarily reflect ongo ing physiologic injury to the brain. Children and youth who have been diagnosed with attention-deficit/hyperactivity disorder or learning dis abilities may require more assistance in returning to school, but are not at increased risk for persistent symptoms. 3,35 Risk factors for poor prognosis include previous concussion his tory, persistent posttraumatic headache, depression, anxiety, persisting vestibular-ocular abnormalities, ongoing cognitive difficulties, preinjury sleep disturbances, increased symptoms with return to school and exercise, and return to high-risk contact sports prior to full recovery. Those who have persistent symptoms should be referred to a con cussion specialty clinic. The team should encompass expertise by a pediatrician, sports medicine specialist neurologists, or neurosurgeon, with allied professional specialties including physiotherapy, clinical psychological, neuropsychology, physiatry, kinesiology, and neuroophthalmology. Delay in seeking a multimodal assessment and treat ment may lead to prolonged functional disabilities. POSTDISCHARGE COUNSELING  REST AND INITIATING PHYSICAL ACTIVITIES Following a concussion, there should be a period of physical rest for 24 to 48 hours. Returning to physical activity can be guided by the four P’s: prioritize activities, plan in advance, pace appropriately, and position in a calm environment. 36 Gradually introduce noncontact and low-risk activities. Avoid activities that exacerbate symptoms. Early return to graduated physical activities results in lower rates of prolonged concussion symptoms at 1 month compared to children and adolescents who adhere to strict rest guidelines until symptom free. 37 The proposed mechanism by which exercise may improve recovery is through the promotion of neuroplasticity mechanisms. Controlled aerobic exercise may improve recovery by restoring normal cerebral blood flow regulation.  RETURN TO LEARN Cognitive rest prevents overtaxing of a functionally injured brain and prevents metabolic overload.

hanism by which exercise may improve recovery is through the promotion of neuroplasticity mechanisms. Controlled aerobic exercise may improve recovery by restoring normal cerebral blood flow regulation.  RETURN TO LEARN Cognitive rest prevents overtaxing of a functionally injured brain and prevents metabolic overload. The degree and duration of cognitive rest vary from person to person. Mental activity should be resumed gradually, even if the person has not returned to baseline. Activities that worsen symptoms should be avoided. Graded return to learn requires accommodation by schools. Providing teachers with specific symptombased guidelines for successful reintegration is helpful (Figure 111-2). Returning to school, even with restrictions, may have significant psy chosocial benefits.  RETURN TO SPORTS A graduated return to sports protocol should be followed. Children and adolescents must be symptom free, off all medications, have a normal For headaches with a migraine component, the use of IV dopamine antagonists (metoclopramide, prochlorperazine, chlorpromazine) and ketorolac may provide temporary relief of symptoms, 32 but does not appear to alter recurrence or persistence. 33 Potential adverse effects of dopamine antagonists include drowsiness, hypotension, and acute dys tonic reactions, particularly in adolescents (Chapter 139, “Headache in Children”). The use of migraine-specific abortive triptan medications may be effective, but should be limited to less than 10 times per month. Do not provide opioids for persistent headaches. Identify headache triggers and relievers if possible. Management strategies should focus on education and expected clinical course. Physical and cognitive overexertion are key factors for worsening headache. Patients with prolonged and debilitating postconcussive headaches should be referred to a neurologist. Preventive medications including gabapentin, valproic acid, topiramate, amitriptyline, carbamazepine, and cyproheptadine may provide symptomatic relief, but require dosage titration and careful monitoring.  NAUSEA Consider ondansetron for significant nausea or difficulty tolerating liq uids. One study suggested that children treated with ondansetron after head injury had lower rates of ED return visits, and ondansetron did not mask serious underlying conditions in those who did not have imaging. Physical and cognitive rest often results in resolution of nausea. Keep the child well hydrated, as dehydration can worsen nausea.  DIZZINESS Concussion-associated dizziness tends to resolve quickly with rest. Dizziness may result from an injury to the vestibular system, the effects of visual disturbances (decreased convergence, accommodation, smooth visual pursuits, eye saccades), decreased exercise tolerance, or cervico genic injury. For prolonged symptoms, refer to a physiotherapist or concussion clinic for targeted exercises including vestibular rehabilitation. A concussion vision specialist may assist in neuro-optometric vision rehabilitation with the goal of improving central-peripheral vision, visual-vestibular and accommodation-vergence integration, pursuit and saccadic eye movement, and convergence ability. Therapy involves strengthening binocularity, reducing visual motion hypersensitivity, and reducing disequilibria. DISPOSITION AND FOLLOW-UP  ED DISPOSITION At this time, there is clinical variation and no gold standard regarding the need for, and length of, ED observation. However, we do know the following: 1. Patients who have been imaged and in whom the CT is negative are at extremely low risk for subsequent deterioration from a bleed. 2. Children who meet PECARN low-risk criteria (Table 111-3) are at very low risk for clinically important traumatic brain injury requir ing intervention. 3.

ver, we do know the following: 1. Patients who have been imaged and in whom the CT is negative are at extremely low risk for subsequent deterioration from a bleed. 2. Children who meet PECARN low-risk criteria (Table 111-3) are at very low risk for clinically important traumatic brain injury requir ing intervention. 3. For children who are symptomatic and not low risk, the PECARN rule recommends observation or CT, but does not specify the dura tion of observation. This author uses around 4 hours of ED observa tion, with CT scan if patient is getting worse and discharge if getting better. Provide discharge instructions regarding signs and symptoms for which to seek immediate medical care. This includes lethargy, irritability, focal deficits, seizures, intractable vomiting, slurred speech, paresthesia, and worsening headache. Caregivers of infants in the first year of life should be warned about the risk of “growing fractures” over the weeks to months following a skull fracture and instructed to see their primary care physician if there is a persistent or worsening palpable defect in the skull >2 weeks after the injury. Patients with intracranial injury and those thought to be at risk for abusive head trauma should be admitted into hospital with appropriate pediatric subspecialty medical, neurosurgical, and nursing resources. Tintinalli_Sec12_p0669-0996.indd 703 8/2/19 7:49 PM

ng palpable defect in the skull >2 weeks after the injury. Patients with intracranial injury and those thought to be at risk for abusive head trauma should be admitted into hospital with appropriate pediatric subspecialty medical, neurosurgical, and nursing resources. Tintinalli_Sec12_p0669-0996.indd 703 8/2/19 7:49 PM 704 SECTION 12: Pediatrics Physical & cognitive rest • Basic board games, crafts, talk on phone • Activities that do not increase heart rate or break a sweat Limit/Avoid: • Computer, TV, texting, video games, reading No: • School work • Sports • Work • Driving until cleared by a health care professional STAGE 2: STAGE 3: Part-time school Increase school time with moderate accommodations. Prior activities plus: • Increase time at school • Decrease accommodations • Homework – up to 30 min./day • Classroom testing with adaptations No: • P.E., physical activity at lunch/recess, sports, standardized testing Communicate with school on student’s progression. Full-time school Full days at school, minimal accommodations. Prior activities plus: • Start to eliminate accommodations • Increase homework to 60 min./day • Limit routine testing to one test per day with adaptations No: • P.E., physical activity at lunch/recess, sports, standardized testing Note: A student is tolerating an activity if symptoms are not exacerbated. Rest Gradually add cognitive activity including school work at home Increase school work, introduce homework, decrease learning accommodations Work up to full days at school, minimal learning accommodations When symptoms start to improve OR after resting for 2 days max, BEGIN STAGE 2 This tool is a guideline for managing a student’s return to school following a concussion and does not replace medical advice. Timelines and activities may vary by direction of a health care professional. Start with light cognitive activity: Gradually increase cognitive activity up to 30 min. Take frequent breaks. Prior activities plus: • Reading, TV, drawing • Limited peer contact and social networking Contact school to create Return to School plan. When light cognitive activity is tolerated: Introduce school work. Prior activities plus: • School work as per Return to School plan Communicate with school on student’s progression. STAGE 1: No: • School attendance • Sports • Work Tolerates 30 min. of cognitive activity, introduce school work at home Tolerates 60 min. of school work in two 30 min. intervals, BEGIN STAGE 3 Back to school part-time

ies plus: • School work as per Return to School plan Communicate with school on student’s progression. STAGE 1: No: • School attendance • Sports • Work Tolerates 30 min. of cognitive activity, introduce school work at home Tolerates 60 min. of school work in two 30 min. intervals, BEGIN STAGE 3 Back to school part-time Part-time school with maximum accommodations. Prior activities plus: • School work at school as per Return to School plan No: • P.E., physical activity at lunch/recess, homework, testing, sports, assemblies, field trips Communicate with school on student’s progression. STAGE 4: STAGE 5: AT HOME AT SCHOOL STAGE 6: Full-time school Full days at school, no learning accommodations. • Attend all classes • All homework • Full extracurricular involvement • All testing No: • Full participation in P.E. or sports until Return to Sport protocol completed and written medical clearance provided Full academic load Tolerates 120 min. of cognitive activity in 30-45 min. intervals, BEGIN STAGE 4 Tolerates 240 min. of cognitive activity in 45-60 min. intervals, BEGIN STAGE 5 Tolerates school fulltime with no learning accommodations BEGIN STAGE 6 Return to School protocol completed; focus on RETURN TO SPORT Adapted from the Return to Learn protocol by G.F. Strong School Program (Vancouver School Board), Adolescent and Young Adult Program, G.F. Strong Rehabilitation Centre. School work only at school

school fulltime with no learning accommodations BEGIN STAGE 6 Return to School protocol completed; focus on RETURN TO SPORT Adapted from the Return to Learn protocol by G.F. Strong School Program (Vancouver School Board), Adolescent and Young Adult Program, G.F. Strong Rehabilitation Centre. School work only at school Return to School www.cattonline.com © BCIRPU. All rights reserved | Version 11: Updated December 2017 FIGURE 111-2. Return to school staged approach. neurologic examination, and have successfully returned to learn before returning to competitive sports. The graded return to sport protocol (Figure 111-3) advances through the following rehabilitation stages: light aerobic activity, more intensive training, sports-specific exercises, noncontact participation, full practice, and finally game play. The athlete must be symptom free during and after exertion before advancing to the next stage, and there should be at least 24 hours between the stages. If symptoms return at any level, the athlete must rest until the symptoms resolve and then begin the protocol level again, at the previous level of symptom-free exertion. The return to play guideline must be individualized and progressive.  GENERAL LIFESTYLE MEASURES Encouraging healthy lifestyle choices is an important aspect of initial care. Physical and cognitive rest assists recovery from concussion through conservation of limited adenosine triphosphate supply. Discuss nutrition (three meals, including protein, and two snacks per day), optimal hydration, and the importance of restorative sleep. Limit screen and device time, and gradually resume normal social activities. Preventing further injury during the time of recovery is essential. Patients should avoid higher-risk recreational activities (cycling, skating, skateboarding) that may result in a second head injury. During recovery, the brain is particularly vulnerable to worsening symptoms, additional concussions, and rarely, second impact syndrome, which results from subsequent low-energy collisions. The injured brain may lose its ability to autoregulate cerebral perfusion, leading to cerebral edema, hernia tion, and potential death.  SLEEP Fatigue and sleep disruption are common following head injury. Day time drowsiness, difficulty falling asleep, and difficulty staying asleep are often experienced. Normalizing sleep patterns hastens recovery. The American Academy of Sleep Medicine recommends that children 6 to 12 years of age sleep 9 to 12 hours per day and adolescents 13 to 18 years of age sleep 8 to 10 hours per day on a regular basis to promote optimal health. 39 This should be appropriately timed and uninterrupted. Sleeping less is associated with attention, behavior, and learning prob lems and an increased risk for accidents, injuries, hypertension, obesity, diabetes, and depression. Excessive sleep is linked to obesity and mental health concerns. 40 Sleep difficulties after head injury may be caused by headache, dizziness, and nausea, but are likely to improve when they are effectively controlled. Provide sleep hygiene strategies. Discuss healthy sleep habits emphasizing the same bedtime and wake time. In the first few hours and days following concussion, daytime naps do not need to be limited. After the initial stages of recovery, lengthy naps should be avoided so as not to interfere with nighttime sleep. If patients have ongoing fatigue, recommend naps <30 minutes long and before 3:00 p.m. Electronic devices should be Tintinalli_Sec12_p0669-0996.indd 704 8/2/19 7:49 PM

aytime naps do not need to be limited. After the initial stages of recovery, lengthy naps should be avoided so as not to interfere with nighttime sleep. If patients have ongoing fatigue, recommend naps <30 minutes long and before 3:00 p.m. Electronic devices should be Tintinalli_Sec12_p0669-0996.indd 704 8/2/19 7:49 PM CHAPTER 111: Minor Head Injury and Concussion in Children 705 turned off during the evening. The sleeping environment should be dark, cool, tidy, and comfortable. The bedroom should be designated exclusively for sleep and should not have any electronic devices. Heavy meals, caffeinated beverages, and excessive sugar should be avoided. A healthy diet with optimal vitamins, minerals, and iron may facilitate endogenous melatonin production. Regular exercise when tolerated should be encouraged earlier in the day, but should be avoided within 2 hours of bedtime. Patients should be exposed to natural light during the day. If sleep strategies are not effective, a trial of melatonin may be indicated; however, its efficacy for concussion has not been studied. As melatonin is not subject to U.S. Food and Drug Administration controls, different preparations may produce variable results. Side effects including daytime drowsiness, headache, dizziness, nausea, depression, and anxiety are uncommon. If melatonin is tried, children should be started at 3 milligrams and adolescents at 5 milligrams approximately 45 minutes before bedtime. Long-acting melatonin should be given if children and adolescents have trouble both falling asleep and staying asleep. Pharmaceuticals including trazadone, mirtazapine, amitriptyline, and quetiapine might be consid ered but should be prescribed by a concussion specialist, neurologist, or pediatrician. Benzodiazepines should be avoided as they cause daytime drowsiness and may interfere with cognition and memory.  FATIGUE Fatigue is often disabling and can be managed by optimizing the home and school environment, including ergonomic furnishings and adjusting lighting. Determine optimal hours for learning and physical activities. Schedule regular periods of rest, break down activities into smaller tasks, and set priorities.  MOOD Mood changes following concussion are often multifactorial and can be transient, persistent, or relapsing. Variables include medical comorbidities, medications, family history of psychiatric disorders, past history of psychiatric disorders, substance abuse, social relationships with family and friends, and cultural factors. Management is multipronged and a referral to a rehabilitation team including mental health specialists and occupational and physical therapists is advised. Psychotherapy focuses on supportive care (providing hope, minimizing misattributions) and behavioral therapy (daily structure, sleep hygiene, exercise–relaxation balance, impulse control, anger management). Cognitive therapy and mindfulness are important components of care. There are no U.S. Food and Drug Administration–approved medications for the treatment of neuropsychiatric symptoms associated with concussion, although psychotropic medications have been used “off label” with some success (antidepressants, mood stabilizers, antipsy chotics, dopamine agonists, β-blockers). REFERENCES The complete reference list is available online at www.TintinalliEM.com. BOTH TOOLS CAN BE USE D IN PARALLEL; HOWEVER, RETURN TO SCHOOL SHOULD BE C OMPLETED BEFORE RE TURN TO SPORT IS COMPLETED If new or worsening symptoms are experienced at any stage, go back to the previous stage for at least 24 hours. You many need to move back a stage more than once during the recovery process. Medical clearance required before moving to stage 5 Light aerobic exercise Walking, swimming, stationary cycling. No resistance training.

r worsening symptoms are experienced at any stage, go back to the previous stage for at least 24 hours. You many need to move back a stage more than once during the recovery process. Medical clearance required before moving to stage 5 Light aerobic exercise Walking, swimming, stationary cycling. No resistance training. The pace of these activities should be at the point where you are still able to have a conversation. Sport-specific exercise Skating drills (ice hockey), running drills (soccer). No head-impact activities. Non-contact drills Progress to complex training drills (e.g. passing drills). May start resistance training. Full-contact practice Following medical clearance participate in normal training activities. Back in the game Normal game play Note: Premature return to contact sports (full practice and game play) may cause a significant setback in recovery. Recovery Increase heart rate Add movement Exercise, coordination, cognitive load Restore confidence assess functional skills Time & Date completed: Yes: Move to stage 2 No: Continue resting Symptoms improve or 2 days rest max? Time & Date completed: Yes: Move to stage 3 No: Return to stage 1 No new or worsening symptoms for 24 hours? Time & Date completed: Yes: Move to stage 4 No: Return to stage 2 No new or worsening symptoms for 24 hours? Time & Date completed: Yes: Move to stage 5 No: Return to stage 3 Symptom-free for 24 hours? Time & Date completed: Yes: Move to stage 6 No: Return to stage 4 Symptom-free for 24 hours? Return to Sport No sporting activity Physical and cognitive rest until symptoms start to improve OR after resting for 2 days max. STAGE 1: STAGE 2: STAGE 3: STAGE 4: STAGE 5: STAGE 6: This tool is a guideline for managing an individual’s return to sport following a concussion and does not replace medical advice. Timelines and activities may vary by direction of a health care professional. www.cattonline.com © BCIRPU. All rights reserved | Version 11: Updated December 2017 FIGURE 111-3. Return to sport staged approach. Tintinalli_Sec12_p0669-0996.indd 705 8/2/19 7:49 PM