210 Pediatric Trauma
Trauma Systems and Trauma Centers
Many studies support the concept that trauma systems and trauma centers improve outcome and that pediatric trauma centers improve outcome for children, especially for those with severe traumatic brain injury. The “Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants and Children and Adolescents,” published in 2003, found sufficient evidence to set seven guidelines for pediatric management. One of the guidelines states, “In a metropolitan area pediatric patients with severe traumatic brain injury (TBI) should be transported directly to a pediatric trauma center if available.” An accompanying option states, “Pediatric patients with severe TBI should be treated in a pediatric trauma center or in an adult trauma center with added qualifications for pediatric treatment.” These guidelines have been endorsed by six medical societies, including the American Association for the Surgery of Trauma and the Society of Critical Care. Over the last 3 decades, thanks to heroic efforts by the American College of Surgery (ACS), many trauma systems with designated adult and pediatric trauma centers have been developed. A recent paper concluded that pediatric trauma center “mortality rates are lower among children admitted directly from the injury scene compared with those admitted by interhospital transfer.”1 Even after allowing for injury severity, Glasgow Coma Scale (GCS) scores, elapsed time between injury and hospital admission, and age, this finding held true. The ACS program provides verification of trauma centers by an excellent outside review process. To date, the ACS has verified 29 level I pediatric trauma centers2 (increased from 13 in 2007). The ACS delineates recommended equipment, staffing, policies, and procedures. Important to the trauma center is a designated trauma director and an active morbidity and mortality conference that is attended by all physician members of the trauma team.
Trauma Teams
Trauma teams are essential to the trauma center. A trauma team refers to all who care for the trauma patient from resuscitation through discharge. Members of the trauma team include the trauma surgeons, emergency department physicians and nurses, critical care physicians and nurses, respiratory therapists, subspecialty surgeons, radiologists, rehabilitation team, social workers, and clergy. A trauma team requires strong hospital commitment and support. To function optimally, multiple policies and procedures that are understood and respected by all members have to be in place. The resuscitation team is usually led by a surgeon and performs best when led by an attending trauma surgeon. The prepared trauma team improves performance in resuscitation as well as outcome of the patient.3
Role of Pediatric Critical Care Physicians
The role of the intensivist in the care of trauma patients has been debated for decades. In 1986, Meyer and Trunkey argued that in most instances, optimal care of seriously injured patients requires “participation between trauma surgeons and critical care specialists, as well as trauma and critical care services. With proper leadership and systems to ensure effective communication between such services, these goals can be achieved. Important secondary goals, in education and research, can also be achieved by such methods.”3 Such attitudes of collaboration and inclusiveness were not always apparent in the 1990s. An editorial in the Journal of Trauma stated, “The American Association for the Surgery of Trauma ratifies the position of the American College of Surgeons Committee on Trauma that the trauma surgeon is and must be responsible for the comprehensive management of the injured patient in the critical care unit, including hemodynamic monitoring, ventilator management, nutrition, and posttraumatic complications.”4 A letter to the editor responding to the editorial stated, “Except for a nod to a team effort, the tenor of your editorial would imply that the trauma surgeon and only the trauma surgeon has all the necessary skills in all areas to care for the multiply injured patient to the exclusion of all others.”5 A reply to the letter stated that the intent of the editorial was not meant to be exclusive and that collaborative participation with all specialties was important. Such debates led to feelings of noncollaboration and exclusion among critical care physicians.
In 1991, the American College of Surgeons Committee on Trauma recommended that an “inclusive” trauma system be developed.6 Atweh advocated that the concept of the inclusive trauma system be broadened to include all phases of injury as well as all the disciplines involved with injuries.7 In 1999, the president of the American Association for the Surgery of Trauma stated, “It is interesting to note who actually provides much of the minute-to-minute and day-to-day care of patients in many trauma centers. The busier the trauma center, the more likely the care is provided by nonsurgeons: anesthesiologists, emergency physicians, critical care doctors of various stripes…. Clearly these workers are needed to manage patients.”8 Cooper wrote, “What we do know, however, is that trauma systems and trauma centers that make special provision for the needs of children achieve better outcomes than those that don’t.”9 He went on to say that the reason for this is more likely to be the specialized system than the surgeon per se and to recommend the development of a fully inclusive trauma system. In October 2002, the Trauma System Agenda for the Future, coordinated through the American Trauma Society, stated that trauma requires a multidisciplinary approach, hospital physicians of all specialties should be included, and appropriate use of all members of the trauma team must be planned.10 The most recent version of “Resources for Optimal Care of the Injured Patient” states, “Appropriately trained surgical and medical trained specialists may staff the pediatric critical care unit.”11
An inclusive system is the right system for pediatric trauma patients, and the pediatric critical care physician should have a significant role. The pediatric critical care physician has the most training and experience in life-support therapies for children, including mechanical ventilation, hemodynamic support, renal replacement therapies, and prevention and treatment of secondary brain injury. As an example, data from San Diego Children’s Hospital (unpublished) show that during an 18-month period, 80 trauma patients required mechanical ventilation. During the same period, 904 nontrauma patients required mechanical ventilation. The critical care physician is also in the critical care unit on a minute-to-minute basis. Studies have shown better outcomes for children in critical care units directed and attended by critical care physicians.12 In our system, the critical care physician and the trauma surgeon conduct daily rounds together, including all trauma patients in the pediatric ICU. All patients are discussed on a daily basis with a neurosurgeon as well. This has built mutual respect, contributed to better patient care, and promoted a good working environment. Inclusive attitudes, teamwork, leadership, standard protocols and policies, an ongoing review of the system, and monthly morbidity and mortality conferences all contribute to the quality of the pediatric trauma center and better patient outcomes.
Initial Resuscitation
Resuscitation of the pediatric trauma patient follows the ABCs (airway, breathing, circulation) of Advanced Trauma Life Support (ATLS) and Pediatric Advanced Life Support (PALS) guidelines. Additional discussion of pediatric resuscitation is provided in Chapter 42 on pediatric neurointensive care. Resuscitation begins in the field with emergency medical service personnel and continues at the trauma center with the designated trauma team.
After successful airway establishment and ventilation, circulation must be assessed. Direct pressure should be applied to any site of active hemorrhage. Pulses, perfusion, capillary refill, heart rate and rhythm, and blood pressure should be evaluated. Intravenous (IV) access, preferably two large-bore catheters, must be obtained rapidly for volume resuscitation. Subgaleal, intraabdominal, intrathoracic, or fracture-related hemorrhage may be life threatening. Heart rate is the most sensitive indicator of hypovolemia in pediatric trauma patients. Young children preserve blood pressure despite losing as much as 25% of their intravascular blood volume.13,14 Thready pulses and altered mental status are evident with loss of 30% to 45% of blood volume. Volume resuscitation begins with crystalloid at 20 mL/kg, with further volume boluses based on the patient’s status. Blood products may be necessary to stabilize patients with hemorrhagic shock. Damage control resuscitation (DCR), or early and aggressive prevention and treatment of traumatic hemorrhagic shock, is advocated by a majority of recent trauma transfusion papers. Basic tenets of DCR include hypotensive resuscitation, rapid surgical control, hemostatic resuscitation with red blood cells, plasma, and platelets in a ratio of 1 : 1 : 1 along with appropriate use of coagulation factors such as rFVII and cryoprecipitate. Fresh whole blood can be used if available. Some refer to hemostatic resuscitation as damage control hematology.15–17 Hemostatic resuscitation can be monitored and fine-tuned with thromboelastography. Hypertonic (3%) saline has been shown to effectively restore intravascular volume while also decreasing cerebral edema and may be used as a bolus of 5 to 10 mL/kg. Blood products should be warmed, because pediatric patients are at high risk for hypothermia.
Hypotension contributes to secondary injury to the brain and other vital organs and must be treated aggressively. In rare cases, vasoactive agents may be necessary in the resuscitation room. Trauma victims who are pulseless at the scene have an almost uniformly fatal outcome.14,18 Prolonged, heroic resuscitative efforts should be avoided in these patients. Patients who have a pulse at the scene but arrest on route or in the emergency department have a slightly better prognosis, and resuscitation should be attempted. Most cardiac arrest associated with blunt trauma is a result of multisystem injuries, including severe brain injury.19 Open chest resuscitation should be considered only in the rare case of penetrating chest trauma, as it has been shown to be of no benefit in blunt trauma.
Specific Injuries and Critical Care Management
Neck Injuries
Penetrating neck and airway injuries occur less frequently in children than in adults. The majority of penetrating airway injuries in children occur in adolescent males.20 Because major structures of the airway, central nervous system, and digestive and vascular systems are contained within the neck, penetrating injuries can be lethal owing to the anatomic structures injured. Wounds from sharp objects or bullets may injure the major vascular structures in the neck, trachea, or esophagus. As a result, penetrating wounds to the face and neck are more likely to require surgical intervention than blunt injuries are. Extensive damage to deep tissues may not be apparent on examination of the wound site. Stab wounds typically produce linear tissue injury that follows a predictable path from the entrance wound into the deeper tissue. Bullet injuries may produce unpredictable tissue damage as the result of deflection and shattering of the projectile throughout the neck. Penetrating injury to any of the major systems usually results in rapid airway compromise and shock.
Although less common than penetrating injuries, blunt neck injuries can be associated with life-threatening airway disruption.21,22 This injury is frequently missed in the presence of concurrent head, face, and thoracic injuries. Also associated with blunt neck trauma are injuries to the cervical spine, esophagus, lungs, and great vessels. Mortality rates of up to 30% are reported for children with these injuries, and half these children die of tracheobronchial rupture within 1 hour of the injury.23
Blunt laryngeal trauma in children is uncommon and frequently unrecognized. The pediatric larynx is characterized by features related to immaturity. Its small diameter, funnel shape, and elastic structure result in significantly greater respiratory problems after trauma compared with adults. Due to its high anterior position in the neck, the larynx of a child is relatively sheltered by the mandible.24 Greater cricothyroid pliability decreases the incidence of fractures, but surrounding tissue edema or blood in the lumen may rapidly produce respiratory difficulties because of the smaller diameter of the airway. The clinical presentation of laryngeal injury in children includes frank respiratory distress with hoarseness, stridor, and palpable subcutaneous emphysema.21 Radiographs of the chest and neck may show subcutaneous emphysema as well. The diagnosis of blunt laryngeal trauma in children is based on history, physical examination, and radiographic studies, followed by flexible or rigid bronchoscopy. CT of the neck adds little to the diagnosis of laryngeal injury. Once a laryngeal injury is suspected, rigid endoscopy in the operating suite should be used to secure the airway as well as delineate and repair the injury. Although adult patients with laryngeal injury frequently undergo an awake tracheostomy under local anesthesia, this is not routine in children. Careful placement of a tracheal tube below the level of injury provides an airway, but this may be difficult to accomplish. Difficulties in securing the airway usually reflect a lack of appreciation of the injury. Typical problems include hematoma and airway distortion, bleeding into the airway, or passage of the tracheal tube into the mediastinum.25
Thoracic Injuries
Thoracic trauma, though rare in children, accounts for 5% to 10% of admissions to trauma centers. In isolation, it carries a 5% mortality rate. This increases fivefold when there is concomitant head or abdominal injury and can exceed 40% when a combination of head, chest, and abdominal injuries is present.26 Potentially life-threatening injuries such as airway obstruction, tension pneumothorax, massive hemothorax, open pneumothorax, flail chest, and cardiac tamponade must be corrected immediately. The last three injuries are relatively uncommon in the pediatric population. Young children have a significantly more flexible thoracic cage than adults do. As a result, compression of intrathoracic organs with blunt trauma may lead to significant parenchymal injuries in the absence of rib fractures. Thus, pulmonary contusions, rather than broken ribs, are far more common in children. In isolation, a broken rib is rarely associated with increased morbidity or mortality.27 An isolated first rib fracture, however, is a potential sign of child abuse28 or may be associated with significant thoracic injury. Isolated cervical rib fracture is very rare but has been associated with backpack usage.29 Multiple rib fractures should alert the clinician to look for underlying injuries in the thoracic cavity. Further radiographic evaluation, such as CT angiography, may be warranted to complete the diagnostic evaluation. Numerous studies have demonstrated that the presence of multiple rib fractures has an approximate 40% mortality rate, often due to the presence of associated multisystem injury.30 Supportive care is the mainstay of rib fracture management. Appropriate analgesia is necessary to promote deep inspiratory effort and prevent atelectasis. Intercostal nerve blocks or epidural analgesia may be helpful when there is respiratory insufficiency but are rarely necessary.
Trauma to the intrathoracic trachea and bronchi is fortunately rare, as 50% of pediatric patients die within 1 hour of tracheobronchial disruption.31 Pneumothorax and subcutaneous emphysema are common findings, but rib fractures are not common. Failure of tube thoracostomy to reexpand the lung and the continued presence of a large air leak denote a tracheal or bronchial disruption. If the site of tracheal or bronchial disruption is within the chest cavity, the endotracheal tube tip should be placed distal to the disruption. This may require bronchoscopy. Selective intubation of the undisrupted mainstem bronchus, followed by one-lung ventilation until the proper resources can be obtained for control of the damaged bronchus, may be required. This must be done rapidly and with great care to avoid extending the tracheal injury. Once the injury is repaired, the patient may benefit from a low-tidal-volume ventilation strategy.
Complete bilateral tracheobronchial disruption in a child with blunt chest trauma has been reported. The child survived after median sternotomy, intubation of both left and right mainstem bronchus, and subsequent cardiopulmonary bypass with subsequent reanastomosis of both left and right mainstem bronchi to the trachea.32
In children, the mediastinum is less fixed than in adults, and the physiologic consequences of tension pneumothoraces may become evident rapidly. Each hemithorax can hold 40% of a child’s blood volume. A chest tube large enough to drain the entire hemithorax without clotting or occluding is necessary. Surgical exploration for hemostasis may be required if the initial chest tube output is 20 mL/kg or greater than 3 to 4 mL/kg/h.33 Inadequate evacuation leads to lung entrapment from a fibrothorax and predisposes the patient to chronic atelectasis. Penetrating injuries may require thoracotomy in the operating room. Anterior penetrating injuries below the nipple line and posterior penetrating injuries below the tip of the scapula warrant exclusion of intraabdominal injuries.
Other thoracic injuries include traumatic asphyxia, chylothorax, and esophageal tears. Esophageal tears occur in less than 1% of children with blunt thoracic injuries. Esophageal lacerations can be diagnosed with flexible esophagoscopy. Lacerations almost always need repair. Mediastinitis can occur and causes with it a risk of mortality.34 Traumatic asphyxia is caused by sudden, severe compression of the chest and upper abdomen and is characterized by craniofacial and cervical cyanosis, edema, and petechiae. Subconjunctival and thoracic wall petechiae also occur. There may be associated respiratory distress, cardiac arrest, and cerebral edema with raised ICP. Retinal hemorrhage, blindness, and orbital compartment syndrome have also been reported.35 Traumatic chylothorax is rare in children but has been reported with blunt and penetrating injury and with child abuse.
Cardiac and Aortic Injuries
Myocardial contusion results from blunt force injury to the chest. The vast majority of pediatric patients with myocardial contusions have multisystem trauma; pulmonary contusion is the most common coexisting injury, found in 50% of patients.36 Hemodynamically significant myocardial contusion is relatively rare in pediatric patients and may present with arrhythmia or ventricular dysfunction. The majority of arrhythmias occur within 24 hours. In a study of 184 pediatric patients with blunt cardiac injury, no hemodynamically stable patient who presented with normal sinus rhythm subsequently developed an arrhythmia or cardiac failure.36 However, there have been case reports of delayed arrhythmia occurring up to 6 days later.
Diagnostic evaluation of myocardial contusion is controversial and is usually based on a series of tests in the appropriate clinical setting. In pediatrics, testing may include a combination of cardiac enzyme determinations, electrocardiography, and echocardiography. Creatine kinase-MB and cardiac troponin-I elevation following blunt trauma has been used to diagnose contusion. Cardiac troponin-I is highly specific for the myocardium, but creatine kinase-MB may be elevated with injury to skeletal muscle. Elevation of troponin-I occurs within 4 hours of injury and peaks within 24 hours. The significance of elevation in a hemodynamically stable patient is unclear, and determination may not be necessary in these patients.37,38 An admission 12-lead electrocardiogram (ECG) is recommended in all patients. Echocardiography may show wall motion abnormalities or ventricular dysfunction. In a small pediatric study, echocardiography was diagnostic of cardiac injury in patients with hemodynamic instability or abnormal chest radiographs who had nondiagnostic ECG and creatine kinase-MB.39
Commotio cordis is an unusual event but is much more common in pediatric patients, with 80% of victims younger than 18 years and 50% younger than 14 years. Blunt trauma to the chest with the impact centered over the heart results in immediate cardiac arrest. It is thought that the narrow anteroposterior diameter of the chest, in conjunction with the increased compliance of the chest wall in pediatric patients, allows a chest-wall blow to be transmitted to the underlying heart. Many but not all cases occur during sports-related activity.40 Blunt chest trauma leads to cardiovascular collapse, with ventricular tachyarrhythmia being the most common arrhythmia. Unlike myocardial contusion, there is no evidence of myocardial injury on autopsy. The survival rate is low, even with prompt resuscitation.40,41
Blunt aortic injury is an extremely uncommon pediatric injury; however, as in adults, it is potentially lethal. The aortic arch is relatively fixed, and the descending aorta is more mobile, making it susceptible to shearing forces during horizontal and vertical deceleration. Three reasons for the rarity of blunt aortic injury in pediatric patients have been proposed. First, most adult thoracic aortic injuries are the result of the driver of a vehicle impacting the steering wheel, with a large force being imparted over a small area. This mechanism does not occur in pediatric patients. Second, blunt trauma in children is often the result of pedestrian-automobile accidents, allowing the force of impact to be widely distributed over the body surface area.42 Third, the breaking stress of the thoracic aorta is inversely related to age43 but is decreased in connective tissue diseases such as Ehlers-Danlos and Marfan syndromes. One of our rare cases of blunt aortic injury occurred in a young child with a connective tissue disorder.
Diagnosis of thoracic aortic injury is similar in children and adults. The pattern of chest x-ray findings is similar, although one study found that depression of the left mainstem bronchus is not as common in pediatric patients. Angiography has been the gold standard for the diagnosis of thoracic aortic injury.44 Helical CT is fast becoming an important diagnostic tool and, when performed properly, has a sensitivity and specificity similar to that of angiography.45,46 Transesophageal echocardiography may also have a role in diagnosis, although its place is less clear. As in adults, successful management of these potentially lethal injuries depends on prompt recognition and treatment.
Abdominal Injuries
The initial evaluation of children with abdominal trauma may include radiographs of the chest, abdomen, and pelvis. At the present time, focused abdominal sonography for trauma is an excellent initial study of the peritoneum and pericardium. Its use is more widespread in adults than pediatrics.47–49 The gold standard for evaluation of children with blunt abdominal trauma is CT with IV contrast. It gives reliable information about solid-organ injuries, the presence of abnormal fluid, the presence of pneumoperitoneum indicating hollow viscus injury, and the retroperitoneal space. Further, organ blood flow and contrast extravasation can be observed. Diagnostic peritoneal lavage is a sensitive test to detect bleeding and a perforated hollow viscus in blunt abdominal trauma; however, its use in pediatrics is limited owing to the success of nonoperative management of solid-organ injuries and rapid CT scanning. Diagnostic peritoneal lavage may be indicated in children who have an emergent operative neurologic injury and require immediate assessment of the abdominal cavity.
Penetrating injury is rare in pediatrics. Virtually all gunshot wounds to the abdomen and lower chest should be treated by mandatory laparotomy. Stab wounds below the nipple line and above the inguinal ligament can be managed selectively by local wound exploration, peritoneal lavage, CT scan, and frequent serial physical examinations to determine the need for laparotomy. A recent paper supports selective nonoperative management of penetrating abdominal injuries in children.50
Liver
Signs and symptoms of hepatic injury include pain and tenderness, abrasions, and contusion of the abdominal wall. Signs of peritonitis due to hemoperitoneum are frequently present. Most isolated liver injuries can be managed nonoperatively. Selective angiography and embolization may control bleeding without the need for operative repair. Operation, however, may be required for hemodynamic instability, continued transfusion requirement, or other associated injuries. The decision to operate is based on the child’s physiologic status and not the graded classification of injury.47 Complications of hepatic injury include hemobilia, abscess, biliary fistula, and bile peritonitis. The potential for delayed bleeding is higher in hepatic than in splenic injury.
Spleen
Nonoperative management is preferable and is similar to the nonoperative management of liver injuries. Angiography and selective embolization should be considered in patients with active bleeding seen on CT.51 Pediatric experience with AE is limited. However, a recent paper reports successful AE in 7 pediatric patients, two spleen (grades IV and V), two liver (grades III and IV), and three grade IV renal injuries.52 Surgical management may be necessary in patients who are hemodynamically unstable, require continued transfusions, or have other associated abdominal injuries. A variety of surgical techniques are available to control bleeding, often without a total splenectomy. The incidence of total splenectomy in pediatric trauma centers is 3%. In patients requiring total splenectomy, there is a risk of post-splenectomy sepsis. In patients splenectomized for trauma, sepsis develops in 1.5%, with a mortality rate of 50%. Postsplenectomy sepsis may occur at any time, but the risk is greatest in the first 5 years of life. All postsplenectomy patients must be immunized.
Duodenum and Pancreas
Most pancreatic injuries are mild.53 They can be managed nonoperatively with nasogastric decompression and parenteral nutrition. When the patient’s condition improves, nasogastric drainage can be discontinued and oral intake begun. Serial enzyme levels and ultrasonography should be performed to identify complications. Patients with severe pancreatic injury may require surgical repair or endoscopic placement of pancreatic duct stents.
Small Intestine
Hollow viscus injuries are far less common than solid-organ injuries in pediatric abdominal trauma patients. Nevertheless, bowel injury may result from even mild abdominal trauma. The mechanism of injury is either compression or shear forces resulting from rapid deceleration. There are two points of fixation to the retroperitoneum that frequently lead to transections: the ligament of Treitz and the cecum. Handlebar blows or direct blows to the abdomen compress the bowel against the vertebral column, resulting in intestinal perforation. In the lapbelt complex, contusions or abrasions of the abdominal wall and lumbar spine injury are associated with bowel perforation. Lapbelt loading generates significant intraabdominal injuries in children. Upper lapbelt loading is associated with liver, spleen, rib, stomach, small-bowel, and large-bowel injuries. Lower lapbelt loading is associated with ribs, small bowel, large bowel, bladder, kidney, and stomach injury. Greater than 40% of Abbreviated Injury Severity Score (AISS) 2+ injuries have small-bowel and large-bowel injuries.54
Damage Control and Abdominal Compartment Syndrome
If the child is hemodynamically unstable despite aggressive resuscitation, a laparotomy for damage control may be required.55 In the presence of the lethal triad of hypothermia, acidosis, and coagulopathy, an immediate definitive surgical repair is unnecessary.56,57 The damage control approach has three stages.58 The first stage is the initial laparotomy, the goal being to prevent ongoing damage by controlling hemorrhage and fecal contamination. Abdominal packing and temporary closure of the wounds with loose retention sutures may be required.59 Definitive surgical repair is postponed until the patient is stabilized. The second stage is carried out in the ICU, with the goals of rewarming, correcting the coagulopathy, and restoring acid-base balance. An abdominal compartment syndrome may develop during the second phase.60 Intraabdominal pressure may be increased by edema, tissue swelling, ascites, and ongoing bleeding. The high pressure may cause cardiorespiratory and renal deterioration. Elevation of the diaphragm produces basilar atelectasis and restriction of lung inflation, which makes ventilation difficult. Increased abdominal pressure can also cause hypoperfusion of the abdominal contents, leading to renal failure and ischemic bowel injury with resultant bacterial translocation. Increased abdominal pressure also may decrease venous return and therefore cardiac output. Treatment of abdominal compartment syndrome is urgent and may require a peritoneal drain or opening of the abdominal wound and placement of a prosthetic silo.61 The third stage involves definitive surgery once the patient is stabilized. Packs are removed, tissues are débrided, bowel anastomoses are performed, and fractures are reduced. Most injured patients are not candidates for damage control surgery. Unstable pediatric patients with severe abdominal injury benefit from this staged approach, which is designed to allow medical resuscitation and avoid continued hypothermia, acidosis, and coagulopathy.
Spinal Injuries
Approximately 5% of all spinal cord injuries occur in the pediatric age group. Common causes in young children include falls and motor vehicle accidents. Recently, inflicted trauma, including gunshot wounds in urban areas, has been identified as a significant mechanism of injury for this age group.62 For older children, sports and other recreational activities such as horseback and bicycle riding have greater etiologic importance.
The head and neck anatomy of a young child resembles that of a “bobble-head” doll, with a relatively large head resting on a small, highly flexible neck. To maintain neutral cervical alignment during transport and initial resuscitation of a child at risk for a spinal injury, a support is often placed under the thorax to achieve torsal elevation, in addition to the use of an appropriately sized cervical collar. Alternatively, a board with an occipital recess may be used for this purpose.63
Cervical spine imaging studies include lateral C-spine, anteroposterior (A-P) C-spine, and open-mouth views, flexion/extension lateral C-spine radiographs, CT, and magnetic resonance imaging (MRI). For the child with symptoms of cervical spine and/or cervical cord injury and for the comatose child, CT imaging, 64-slice, and/or MRI are now recommended. A number of recent papers in the literature discuss optimal C-spine imaging.64,65 Some of these are discussed in the section on imaging in this chapter.
Prospective randomized multicenter trials of pharmacologic agents for the treatment of acute spinal cord injury in children younger than 13 years have not been carried out. However, data from adult studies have been extrapolated and are commonly used to dictate management schemes in children. Methylprednisolone is administered within 3 hours of injury as an initial IV bolus of 30 mg/kg to run over 15 minutes, followed by an infusion of 5.4 mg/kg/h to run over 23 hours.66 If the initial administration is between 3 and 8 hours after injury, the infusion is continued for 48 hours. Methylprednisolone treatment is not initiated more than 8 hours after injury.67 Recent studies, however, show no benefit of high-dose methylprednisolone for complete and incomplete spinal cord injury and suggest very limited use of methylprednisolone because of the high incidence of pneumonia.68,69
Closed Head Injuries
It is estimated that each year, 2685 children between the ages of 1 and 14 die from TBI; 37,000 are hospitalized, and 475,000 are treated in hospital emergency departments.70 TBI costs per year for the age group 1 to 19 years is over $2.5 billion.71 TBI is caused by linear and inertial forces resulting in an impact injury.72 This is the primary injury. It includes hematomas, lacerations, and axonal shearing and is often described as irreparable. Secondary injury refers to the injury that occurs after impact. It is considered both preventable and potentially reversible. Pathologic alterations in respiratory, hemodynamic, and cellular function occur, which may lead to secondary injury and cell death. The pathways to neuron death include inadequate oxygen and nutrient supply secondary to hypoxia and decreased cerebral blood flow. Decreased cerebral blood flow can occur secondary to hypotension, decreased cardiac output, raised ICP, and cerebrovascular dysregulation, including endothelial dysfunction, vasospasm, and microthrombus formation. Elevated ICP occurs secondary to mass lesions, cerebral edema, and increases in cerebrospinal fluid volume and cerebral blood volume. Other pathways to neuron death include excitotoxicity, energy failure, inflammation, oxidative stress, and apoptosis. Present therapies are directed primarily at supporting oxygenation, blood pressure, and cardiac output and at controlling ICP.73
After an exhaustive literature review, the “Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents”74 found insufficient evidence to support any standards of care but sufficient evidence to support some guidelines for care: transfer of children in a metropolitan area with severe TBI to a pediatric trauma center, avoidance of hypoxia, correction of hypotension, maintenance of cerebral perfusion pressure greater than 40 mm Hg in children, a recommendation against the continuous infusion of propofol for either sedation or the control of intracranial hypertension, a warning against the use of corticosteroids, and a recommendation against the prophylactic use of antiseizure medication. Evidence was sufficient to support 17 care options and a flow diagram.
Initial stabilization requires support of the ABCs. The airway must be maintained and breathing supported to prevent hypoxemia and hypercarbia. Hyperoxia and brief aggressive hyperventilation are indicated during the initial resuscitation if the clinical examination reveals signs of herniation or acute neurologic deterioration. Normotension or mild hypertension and mild hypervolemia are indicated to support cardiac output and cerebral blood flow. Fluids, sedation, and vasoactive agents must be judiciously administered. Hypertonic saline may be advantageous as a resuscitation fluid for patients with shock, especially those with raised ICP. All children with a suspected TBI, history of loss of consciousness, altered level of consciousness, focal neurologic signs, evidence of a depressed or basilar skull fracture, a bulging fontanelle, or persistent headache and vomiting should have a head CT.72 Surgery is indicated for significant mass lesions. ICP monitoring is indicated for patients with a GCS score less than 8. Even with a normal CT scan, 10% to 15% of patients with a GCS score less than 8 have elevated ICP. A physician may also choose to monitor ICP in certain conscious patients whose CT scans indicate a high potential for decompensation or in patients in whom neurologic examination is precluded by sedation or anesthesia. Physicians should be aware that in a few patients with normal CT findings and elevated ICP, the only symptoms are moderate to severe headaches, vomiting, and lethargy.
Initial treatment for elevated ICP includes mild hyperventilation, with partial pressure of carbon dioxide (PCO2) 35 to 40 mm Hg, sedation and analgesia, ventriculostomy drainage, and muscle relaxants. Sedation can be accomplished with low-dose fentanyl, 1 to 2 µg/kg/h, dexmedetomidine, 0.4 to 1 µg/kg/h, intermittent doses of benzodiazepines or barbiturates, or a low continuous infusion of pentobarbital or sodium thiopental at 1 mg/kg/h. If ICP is not controlled, a repeat CT should be obtained and hyperosmolar therapy begun. Osmolar agents include mannitol and hypertonic saline. Hypertonic saline appears to have several advantages over mannitol.73 A continuous infusion of hypertonic saline allows consistent control of osmolality, potentially minimizing the frequency and magnitude of ICP spikes.75 Hypertonic saline supports mean arterial pressure and cardiac output. It also has beneficial vasoregulatory properties and may have beneficial effects on immune and inflammatory responses.73 The guidelines have found sufficient evidence to include hypertonic saline as an option under hyperosmolar therapy and to regard it as first-tier therapy. Recommendations for osmotherapy include mannitol (also as a first-tier therapy) given as a bolus (0.25-1 g/kg) provided serum osmolarity is less than 320 mOsm/L, and hypertonic saline (3%) administered as a continuous infusion (0.1-1 mL/kg/h). The appropriate dose is the minimum dose required to keep the ICP less than 15 to 20 mm Hg. The dose may be increased provided serum osmolarity is less than 360 mOsm/L. A recent paper verified the safety of continuous hypertonic saline while recommending future studies comparing bolus to continuous dosing.76 Additional areas of investigation in TBI therapy include hypothermia, role of decompressive craniotomy, monitoring of brain tissue oxygenation and cerebrovascular pressure reactivity, continuous versus intermittent drainage of CSF, glycemic control, use of neuroprotectants such as erythropoietin and progesterone among others, and stem cell therapy.
High-dose barbiturate therapy, hyperventilation to a PCO2 less than 30 mm Hg, moderate hypothermia, and decompressive craniectomy are regarded as second-tier therapies. It is prudent to obtain a repeat CT of the head each time a significant increase in medical therapy is required. In adults with severe TBI, an aggressive management strategy has been associated with a lower mortality rate, with no significant difference in functional status at discharge among survivors.77