Pediatric Trauma

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210 Pediatric Trauma

Injury is the leading cause of medical expenditure for children aged 5 to 14 years. In addition, traumatic injury accounts for approximately 300,000 childhood hospitalizations per year and, in the year 2000, was responsible for more deaths in the 1- to 14-year age group than all natural causes combined. This chapter focuses on trauma-related topics from the viewpoint of a pediatric critical care physician.

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.

Upon arrival, the airway is assessed for patency and maintainability. The airway may need to be secured if the patient has experienced head, thoracic, abdominal, or airway trauma. Adequate airway control must be obtained while maintaining cervical spine immobilization. These patients are at risk for aspiration secondary to absent or diminished laryngeal reflexes and delayed gastric emptying. Most trauma patients should be orally intubated with direct cricoid pressure.

Many pharmacologic agents are available for rapid-sequence intubation, similar to adult resuscitation. Doses are adjusted for patient weight. The reason for intubation as well as the type of injuries present dictate the medications used. Tracheal tube placement should be confirmed by auscultation of the abdomen and both sides of the chest, checking the position at the lips, and palpation of the cuff in the suprasternal notch. Placement should also be confirmed by end-tidal carbon dioxide monitoring and radiography. The patient’s heart rate, blood pressure, oxygen saturation, color, and perfusion should be continuously monitored. Once the airway is secure, ventilation should be evaluated. If unequal breath sounds are noted and the tracheal tube is in the correct position, a hemothorax, pneumothorax, or plugging of a large bronchus may be present. Tracheal deviation, though rare, may help with the diagnosis of tension pneumo- or hemothorax. Breath sounds are transmitted easily in children, and a simple pneumothorax is often not apparent until a chest radiograph is obtained. Tube thoracostomies are placed as needed. Flail chest is rare in pediatrics owing to the flexibility of the rib cage. Ventilation should be maintained with 100% oxygen during resuscitation.

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.

The neurologic examination should focus on the level of alertness, GCS score, pupillary response, focal signs of spinal cord injury, and signs of increased intracranial pressure (ICP). Subjects with a GCS score of 8 or less or with a waning mental status should be intubated using rapid-sequence intubation. Noncontrast head computed tomography (CT) should be performed immediately. Cooling the head-injured patient remains an interesting and controversial therapy.

All trauma patients are undressed and exposed for a full examination. Children rapidly lose heat and should be warmed with lights and blankets.

A secondary survey with full physical examination and radiographs as needed should follow the primary survey and stabilization. Once the patient is stabilized and resuscitation is complete, the team decides on a disposition.

Specific Injuries and Critical Care Management

Neck Injuries

Injuries to the airway in children can be rapidly life threatening. Small airway diameter combined with penetrating or blunt injury to the neck can produce rapid airway obstruction. Children are at greater risk than adults for spinal and major vascular injury from neck trauma. Death from airway injury may occur secondary to disruption of the airway at any level.

Clinically, the neck is divided into three anatomic zones, and management of traumatic airway injuries largely depends on which zone contains the injury. Zone 1 extends from the level of the clavicles up to the cricoid cartilage. Injuries to this area may involve the apex of the lung; trachea; subclavian, carotid, and jugular vessels; thoracic duct; esophagus; vagus nerve; and thyroid gland. Patients suffering zone 1 injuries typically exhibit hypotension, because the great vessels are often injured. Zone 2 encompasses the area from the cricoid to the mandible. Injuries to this area are the easiest to detect. Active bleeding can be reduced by direct pressure. The previous approach of mandatory operative management for zone 2 penetrating injury has been replaced by one of selective surgical exploration of wounds after clinical, endoscopic, and radiographic evaluation. Zone 3 extends from the angle of the mandible to the base of the skull. The oropharynx, jaw, and teeth are located within this area. Mandibular fractures in children manifest as malocclusion of the biting surfaces of the teeth and are usually associated with dental injuries. Injury to the chin associated with tympanic membrane perforation or hemotympanum is associated with an occult fracture of the mandible. Orotracheal intubation is not usually problematic in children with mandibular fractures unless there is copious oral hemorrhage. The neck is further divided into anterior and posterior regions. The anterior region contains the oropharynx, trachea, esophagus, and major vascular structures. The posterior neck contains the spine, spinal cord, and large neck muscles.

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.

Penetrating injury to the esophagus may not be immediately apparent but can produce delayed morbidity due to mediastinitis. Investigation of anterior neck injuries that involve the trachea should always include evaluation of the esophagus for perforation. Esophageal perforation should be suspected if fever, elevated white blood cell count, and subcutaneous air in the neck occur in the days following a traumatic neck injury. Management of the perforation requires prompt surgical repair of the esophagus, drainage of the surrounding soft-tissue infection, and IV antibiotics.

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

Pulmonary contusion may occur with or without the presence of overlying rib fractures or chest wall injury. Symptoms include tachypnea, dyspnea, cyanosis, hemoptysis, and respiratory failure. The initial chest radiograph may not demonstrate this injury, and repeat x-rays may be necessary to reveal the infiltrates. Excessive fluid administration should be avoided. Mechanical ventilation may be necessary. Acute respiratory distress syndrome (ARDS) is uncommonly associated with pulmonary contusion, but it may develop. In rare cases, there may be severe pulmonary hypertension.

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

Traumatic injury to the heart and great vessels is significantly less common in pediatric patients than in adults. Most injuries are the result of blunt trauma; penetrating injuries are rare and carry a higher mortality rate.

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

In addition to myocardial contusion, structural damage such as traumatic ventriculoseptal defect, valve injury, ventricular rupture, or aneurysm may occur with blunt chest trauma. The management of all blunt cardiac injury is largely supportive, with operative intervention as needed for significant structural damage. Continuous ECG monitoring is recommended.

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

More than 90% of abdominal trauma in pediatrics is the result of blunt trauma; penetrating trauma accounts for only 5% to 10% of injuries. After initial resuscitation, evaluation of specific injuries begins. It is important to know the mechanism of trauma to appreciate the potential abdominal injuries. A nasogastric or orogastric tube as well as a Foley catheter should be placed during abdominal evaluation, because dilatation of the stomach and bladder can cause significant pain, interfering with the examination. Inspection of the abdomen may reveal external evidence of trauma suggestive of an underlying injury. Evaluation of abdominal tenderness is important but may be an unreliable finding in a child with lower rib fractures, contusion or soft-tissue injury to the abdominal wall, or pelvic fracture. Auscultation with absent bowel sounds indicates ileus and may suggest underlying gastrointestinal (GI) injury. The pelvis should be examined by compression. Rectal examination should always be performed. If there is blood at the urethral meatus, perineal hematoma, or pelvic instability, a serious pelvic injury should be suspected. Hematuria is indicative of genitourinary injury.

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

The spleen is the organ most frequently injured in blunt abdominal trauma. Ecchymosis, pain, and tenderness over the left upper quadrant are suggestive of splenic injury. Left shoulder pain may be present as a result of diaphragmatic irritation. Abdominal CT is recommended to determine the extent of injury as well as the presence of hemoperitoneum and other associated injuries.

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

The duodenum and pancreas are considered as a unit because they share a blood supply and are connected in the retroperitoneum. For these reasons, managing pancreaticoduodenal injuries is complicated. The most common cause of injury is blunt midepigastrium trauma from a blow, automobile crash, or bicycle handlebar. The diagnosis of pancreaticoduodenal injuries can be achieved using chemical markers and imaging studies. Serum amylase and lipase are indicators of pancreatic injury, but amylase levels may be elevated due to injuries to other organs, including the salivary glands. Ultrasonography and CT are the preferred imaging studies to delineate the pancreas. Duodenal perforations can be diagnosed using upper GI studies with water-soluble contrast or CT scan with oral contrast, in which free air or extravasation may be seen.

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.

Several complications may occur after pancreatic injury, including pleural effusion, bile duct obstruction, and pancreatic pseudocyst. Pancreatic pseudocyst occurs in one-third of patients.

Most duodenal injuries are lacerations that can be treated by simple débridement and primary repair. For extensive duodenal injuries in which more than 50% of the circumference is affected, the blood supply is compromised, or bile duct/pancreatic injury is present, an aggressive surgical approach may be necessary. Duodenal hematoma results from blunt abdominal trauma associated with rapid deceleration or from a direct blow to the upper abdomen. It may present a day or more after injury as vomiting or a large amount of nasogastric drainage. It is easily diagnosed by ultrasonography or upper GI studies. The resultant intestinal occlusion should be treated by nasogastric decompression and parenteral nutrition until the obstruction resolves. If it fails to resolve within 3 weeks, an operation should be considered.

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

Identification of patients with a bowel injury may be challenging. Obtaining a detailed history of the mechanism of injury may prevent a delay in diagnosis and late complications. Detection of peritoneal signs may be difficult owing to distracting pain from the abdominal wall and back injury. If there is also a solid-organ injury, peritoneal signs and symptoms may be interpreted as solely from the associated hemoperitoneum. There is no completely reliable imaging study available to detect intestinal injury. CT may show nonspecific findings suggestive of bowel injury. Serial clinical examinations and repeat CT scanning are important to diagnose injury in a timely fashion. Diagnostic peritoneal lavage may also play a role. Patients should receive nothing by mouth until a bowel injury is no longer suspected.

Diaphragm

Diaphragmatic rupture is the consequence of direct blunt trauma over the lower thorax and abdomen. The injury is most frequent on the left side. Contusion or abrasions of the upper abdomen, bowel sounds in the chest, and respiratory distress are the classic findings of a traumatic diaphragmatic rupture. A chest radiograph may show bowel and the nasogastric tube in the thorax. The diagnosis may be confirmed by upper GI studies, ultrasonography, CT, and/or thoracostomy/laparoscopy. Laparotomy allows proper repair of the diaphragmatic defect and assessment of other organs.

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.

Genitourinary Injuries

Genitourinary trauma is common and occurs in 12% of injuries in children. It rarely results in death, but when death does occur, it is usually due to associated injuries. The unique characteristics of a child’s anatomy predispose to genitourinary trauma. The kidneys are proportionally larger, the abdominal musculature underdeveloped, and the ribs less ossified than in adults. In addition, the underdeveloped renal capsule and Gerota’s fascia increase the likelihood of laceration, hemorrhage, and urine extravasation.

The mechanism of injury is usually blunt force (98%) and has a high association with pelvic trauma. Preexisting renal disease (neoplasms and duplicated collecting systems) predisposes to renal injury and is found in 20% of cases of documented renal trauma. Findings suggestive of genitourinary trauma include flank or abdominal tenderness, perineal injury, blood at the urinary meatus, mobile or displaced prostate, and gross hematuria.

Renal injuries are classified according to severity. Parenchymal injuries not involving the collecting system or renal vessels constitute 85% of renal injuries (grades I to III). Injuries to the collecting system or renal vessels account for 10% of renal injuries (grade IV), and the most severe injuries (grade V), including a shattered or devascularized kidney, constitute 5% of renal injuries.

Treatment goals for pediatric renal trauma include preserving kidney tissue and minimizing patient morbidity. Minor injuries rarely require surgery and are treated expectantly. Limited hospitalization with decreased activity until hematuria has resolved is all that is necessary. Imaging at 6 to 8 weeks following discharge is recommended.

Surgical intervention should be reserved for patients with major injuries and hemodynamic instability from persistent bleeding. An imaging study (CT) or intraoperative intravenous pyelogram (IVP) should be performed to assess the contralateral kidney before undertaking renal exploration. Controversy exists over the management of major injuries in patients who have normal vital signs. Even in the case of urine extravasation without urethral injury, expectant treatment with frequent imaging studies at 5- to 7-day intervals is recommended. Nonoperative management of pediatric renal trauma has become the preferred approach in managing blunt renal injuries.

Penetrating renal injuries secondary to gunshot wounds should be explored because of the high incidence of associated injuries. Surgical treatment for stab wounds with suspected renal involvement should be based on the severity of hemorrhage and both clinical and imaging evidence suggesting intraabdominal injury.

Renovascular injuries generally occur in patients who have sustained life-threatening multisystem injuries. The mechanism of renovascular injury is thought to be deceleration with initial injury and arterial thrombosis. This occurs more frequently on the left side. The diagnosis is established with either contrast-enhanced CT or arteriography. Successful revascularization depends on the length of renal ischemia, extent of vascular injuries, and extent of associated injuries. Renal vein injuries are repaired in most cases. Repair of penetrating renal artery injuries is most successful if the ischemic time is less than 8 hours. Blunt arterial injuries are associated with the lowest rate of renal preservation and are most often treated by nephrectomy when they are unilateral.

Pelvic Fractures

Pelvic fractures are a marker for significant trauma and are often associated with other injuries. Pelvic fractures occur in approximately 2% of all blunt abdominal injuries, and 20% of those with pelvic fractures have intraabdominal injuries. Mortality varies from 10% to 50% and is often due to associated injuries. The most common mechanisms are falls, crush injuries, and motor vehicle accidents. Clinically, the diagnosis is suggested by pain with anterior or lateral compression of the pelvis. Other findings may include perineal ecchymosis, blood at the urinary meatus or on the rectal examination, disruption of the rectal wall with mass effect due to bony fragments, or displacement of the prostate.

Evaluation of pelvic trauma begins with a pelvic radiograph and should include CT. Morbidity is lower in children than in adults. Treatment usually consists of bed rest, immobilization, and blood loss replacement. Severe injuries with significant blood loss may require prompt intervention and immobilization, wrapping the pelvis with a bed sheet, or application of an external fixation device. Selective embolization can also provide hemostasis.

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

Initial assessment dictates the need for imaging studies. An awake, communicative child without midline cervical tenderness, intoxication, decreased level of consciousness, focal neurologic deficit, or a painful distracting injury does not require spinal imaging studies.

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

In a child with a spinal cord injury, emphasis is placed on maintenance of optimal physiologic homeostasis. Because of loss of sympathetic tone, IV pressor agents are frequently required in addition to crystalloid and colloid solutions to maintain age-appropriate blood pressure and cardiac output. Intubation may be necessary with high cervical spine injuries because of respiratory compromise. Avoidance of unnecessary neck manipulation is essential.

After initial resuscitation and the identification of spinal injuries, urgent neurosurgical and orthopedic consultation is indicated. Closed reduction and initial stabilization of these injuries are frequently performed in the ICU. Halo rings can be placed with acceptably low morbidity in the ICU setting, even in infants; they can be attached to weighted traction mechanisms for closed reduction if necessary and converted to halo jackets to maintain alignment. The need for and timing of internal surgical stabilization should be discussed in the context of the child’s concomitant multisystem issues. Hypothermia and hypertonic saline are therapies that are being evaluated.

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.

ICP monitoring with a ventricular catheter, an external strain gauge transducer, or a catheter tip pressure transducer is considered accurate and reliable. Ventriculostomy allows cerebrospinal fluid drainage in addition to ICP monitoring and appears to decrease the magnitude of other therapies needed. In patients with a significant cerebral contusion, an ICP monitor on the same side may more accurately reflect the ICP near the contusion.

ICP in children and adolescents should be kept less than 20 mm Hg. In young infants with open fontanelles and sutures and in older children with large diastatic skull fractures, controlling the ICP at less than 10 to 15 mm Hg may be wise.

The guidelines recommend a cerebral perfusion pressure greater than 40 mm Hg in children with TBI. It may be better to maintain cerebral perfusion pressure according to an age-related continuum between 45 and 70 mm Hg.

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

Organ Failure

Acute Respiratory Distress Syndrome

Trauma can result in lung injury and respiratory failure, the most severe of which is ARDS. Posttraumatic respiratory failure results from both direct and indirect injury to the respiratory system. Direct injuries include aspiration of gastric contents, near drowning, smoke inhalation, and pulmonary contusion. Lung injury also occurs indirectly as a consequence of systemic insults such as shock, sepsis, massive transfusion, fat embolism syndrome, or the systemic inflammatory response syndrome (SIRS). For non–massively transfused trauma patients, plasma administration has been associated with a substantial increase in ARDS.⁷¹ ARDS is an acute and progressive respiratory disease of a noncardiac nature associated with diffuse bilateral pulmonary infiltrates and hypoxemia. The definition includes a ratio of arterial oxygen tension (PaO₂) to inspired oxygen fraction (FIO₂) less than 200.

The pathologic findings in ARDS are the result of a complex sequence of cellular and biochemical changes that lead to damage of the endothelial membranes. The specific roles and relative importance of leukocytes, complement activation, prostaglandin release, oxygen radicals, and other mediators of vascular damage are not completely understood. Neutrophils are thought to be an important mediator. This is supported by clinical findings of transient leukopenia in ARDS patients and increased numbers of neutrophils in lung tissue and bronchoalveolar lavage fluid. Blunt trauma enhances the migratory capacity of neutrophils in response to interleukin-8, potentially increasing the risk of ARDS.⁷⁸

The incidence and outcome of ARDS in the pediatric trauma population have not been well studied. In a series of 1989 pediatric trauma patients over an 8-year period with blunt trauma (79%), penetrating trauma (12%), and burns (9%), the overall risk of ARDS was 14%, with a mortality rate of 24%. In those patients with burns, all intubated patients developed ARDS, and the mortality rate was 42%.⁷⁹ In a study of adult patients with severe head injury, those patients who developed acute lung injury had a significant increase in mortality (38% versus 15%) and a worse neurologic outome.⁸⁰ In our trauma practice, ARDS is seen most often in association with SIRS in patients with severe TBI, often as cerebral edema is improving (unpublished data).

ARDS management in pediatrics has focused on minimizing iatrogenic lung injury and on adjuncts to mechanical ventilation. Both oxygen and mechanical ventilation can be injurious to the lung. Oxygen causes oxidative damage and absorptive atelectasis, with chronic exposure to high inspired concentrations of oxygen creating a pathologic picture indistinguishable from ARDS. In both animal and human studies, toxic reactions to oxygen occur commonly with the use of FIO₂ greater than 0.5, and these effects worsen when excessive oxygen is used for longer than 24 hours. Mechanical ventilation also causes lung injury due to increased shear forces applied in the terminal airways. The higher the tidal volumes used to ventilate patients, the greater the stresses and the larger the risk of secondary lung injury. These stresses on the terminal airways and pulmonary endothelium incite pulmonary edema, surfactant dysfunction, decreased compliance, hyaline membrane formation, and impairment of gas exchange.

Ventilatory strategies focus on decreasing iatrogenic lung injury by limiting oxygen concentration and using high-frequency or oscillatory ventilation. Permissive hypercapnia (allowing PCO₂ 45-60 mm Hg or higher) is also practiced when the patient’s condition allows. The strategy of “low-stretch” ventilation has been shown to decrease morbidity and mortality in pediatric ARDS.^81,⁸² Additional support for low-volume, low-pressure ventilation comes from the National Institutes of Health ARDS Network trial comparing 6 mL/kg versus 12 mL/kg tidal volumes in patients with ARDS. Mortality in the low-tidal-volume group was 31.3%, versus a mortality of 39.8% in the higher-tidal-volume group.⁸³ Paulson and colleagues used a high-rate, low-tidal-volume (3-5 mL/kg) strategy on 53 children with severe ARDS and had a survival rate of 89%.⁸¹ Hypercapnia is well tolerated, except in patients with TBI with intracranial hypertension or those with severe pulmonary hypertension. In addition to low-stretch ventilation strategies, helium-oxygen mixtures are being used to improve gas exchange at lower peak pressures. For patients who fail support with mechanical ventilation, extracorporeal membrane oxygenation support can be employed. There are many other adjuncts to ventilation that may decrease the morbidity and mortality of ARDS. These adjuncts include prone positioning, inhaled nitric oxide (NO), surfactant, steroids, immunomodulation, antiinflammatory agents, and immunonutrition; all remain under investigation.

Prone positioning has been used to improve oxygenation in ARDS patients. The improvement may be a result of the redistribution of ventilation or lung perfusion with improved ventilation/perfusion matching. Recent papers conclude that prone ventilation reduces mortality in patients with severe ARDS.^76,⁸⁴ Prone positioning does improve oxygenation and is possible in patients with a wide variety of injuries as well as support lines. If it is not possible, a roto-bed with rotation to 45 to 180 degrees can be used with similar benefit to oxygenation, allowing a decrease in ventilation pressures.

Inhaled NO has potent pulmonary vasodilatory effects and is potentially useful in ARDS, especially in a few cases that have a marked increase in pulmonary vascular resistance. Dellinger and coworkers conducted a randomized trial of inhaled NO versus placebo in 177 patients with ARDS.⁸⁵ Although an acute increase in PaO₂ was observed in 60% of patients receiving NO versus 24% of placebo-treated patients, this did not confer any advantage in overall survival. Several other randomized studies of inhaled NO have had similar results.⁸⁶ The use of inhaled NO delivered during high-frequency oscillatory ventilation in patients with ARDS resulted in a significant increase in arterial oxygenation.⁸⁷

Shock

Shock in children sustaining trauma is most commonly a direct result of hemorrhage, but it can occasionally be the result of tension pneumothorax, spinal cord injury, cardiac tamponade, myocardial contusion, or sepsis. Direct tissue injury and hemorrhage play roles in early shock, while inflammation and altered immune function can result in SIRS, multiple organ failure, and septic shock later in the course.

Children and adults respond differently to hemorrhagic shock. Children have remarkable compensatory mechanisms in response to hypovolemia. Children maintain cardiac output by increasing the heart rate more than the stroke volume. Hypotension is a relatively late sign of traumatic shock in children; therefore, relying on hypotension as an indicator for fluid resuscitation can be deleterious. Tachycardia and signs of end-organ hypoperfusion, such as altered mental status, cool distal extremities, and decreased urine output, may be the primary clinical signs of shock in an injured child.

The focus of therapy for shock in an injured child should be on restoration and maintenance of adequate oxygen delivery and organ perfusion. Hemodynamic monitoring of central venous pressure and direct arterial blood pressure, as well as cardiac output, may be necessary. In addition, clinical parameters such as base deficit,⁸⁸ serum lactate,⁸⁹ and measured creatinine clearance are useful indirect measures of adequate end-organ perfusion and may have prognostic value.^88,⁹⁰ Appropriate therapy of early shock resulting from trauma can alleviate the development of SIRS and multiple organ failure later. Resuscitation with hypertonic saline in two animal models of trauma and hemorrhagic shock was shown to attenuate neutrophil-mediated organ injury; specifically, this occurred in the lung, where much of the inflammation of SIRS occurs, and in the intestine, which is thought to be a major source of neutrophil activation following ischemia.^91,⁹² A recent paper demonstrated an increase in survival in ARDS patients receiving hypertonic saline during resuscitation if those same adult patients had required 10 units or more of packed red blood cells in the first 24 hours.⁹³ There may also be a role for stress-dose steroids following hemorrhagic shock, because sustained adrenal impairment is frequently seen and may be related to the inflammatory consequences and vasopressor dependency of hemorrhagic shock.⁹⁴

The tissue ischemia and hypoperfusion associated with shock result in alteration of cellular function due to oxygen and nutrient deficiency, eventually leading to activation of inflammatory mediators. A current model of SIRS and multiple organ failure in trauma patients is the “two-hit hypothesis.” The initial hit is the shock-resuscitation or ischemia-reperfusion phase, which activates neutrophils, making them more susceptible to an exaggerated immune response to late inflammatory stimuli, the second hit.^95,⁹⁶ Barbiturates and hypothermia, both used to treat severely head injured patients, suppress neutrophil function, increase infectious risks, and may contribute to the late inflammatory stimuli leading to SIRS and multiple organ failure. It may be that severe TBI with release of cytokines itself triggers SIRS. The inflammatory mediator response to trauma that leads to SIRS and multiple organ failure has been proposed as a “three-level model,” with mediators acting at the levels of cells, organs, and the organism. Immune modulation has been the focus of current research in trauma with regard to the late sequelae of SIRS and multiple organ failure.⁹⁷

Renal Failure

Renal failure in pediatric trauma patients early in the hospital course is most often due to organ injury from initial shock or from primary injury to the kidney, its vasculature, or urinary outflow tract. Anatomic reasons for renal insufficiency should be delineated by radiographic evaluation. One kidney is sufficient for adequate function; therefore, clinically evident renal failure requires injury to both kidneys or shock.

Renal failure that develops during the course of hospitalization is most commonly secondary to SIRS and multiple organ dysfunction syndrome. In addition, rhabdomyolysis, contrast nephropathy from imaging studies, or nephrotoxicity from medications may occur. Abdominal compartment syndrome and renal vein thrombosis also can lead to renal failure. High-dose mannitol, 0.25 gm/kg/h, as an infusion over 58 ± 28 hours, has been associated with renal failure.⁹⁸ This is thought to be secondary to renal vasoconstriction. There is also concern that hypernatremia can cause renal failure. However, in studies using hypertonic saline for control of intracranial hypertension, renal failure did not occur unless SIRS with multiple organ failure was also present.⁷⁵

Signs and symptoms of acute renal failure are due to the accumulation of urea, electrolyte derangements, and volume overload. The first clinical features may be oliguria, hyperkalemia, and elevations in blood urea nitrogen (BUN) and creatinine. The laboratory evaluation of acute renal failure should include measurements of BUN, creatinine, electrolytes with phosphate, magnesium, and calcium, urinalysis, and urine electrolytes. Creatinine clearance should be measured to estimate glomerular filtration rate. Daily 4-hour creatinine clearances are helpful in detecting early changes in renal perfusion and function. Microscopy is necessary to differentiate hemoglobinuria or myoglobinuria from hematuria, and additional tests such as creatine phosphokinase can aid in the confirmation of crush injuries threatening renal function. A recent large multicenter prospective cohort of trauma patients showed that acute kidney injury (AKI; RIFLE [risk, injury, failure, loss, end-stage renal disease] criteria) was associated with an independent risk of hospital death in a dose-response manner even in patients with mild AKI.⁹⁹

Prevention of acute renal failure includes aggressive resuscitation from shock and continued maintenance of cardiac output and organ perfusion pressure. In addition, minimizing and monitoring of nephrotoxic drugs may be helpful. Many agents have been used to prevent and treat acute ischemic or nephrotoxic renal injury. They include furosemide, mannitol, calcium channel blockers, and dopamine, most without benefit.¹⁰⁰ Although diuretic therapy may convert oliguric to nonoliguric acute renal failure, there is no evidence that patient outcome is improved. Prehydration and prophylaxis with theophylline or N-acetylcysteine has been shown to reduce the risk of contrast nephropathy and may be of benefit for children undergoing contrast scans who already have or are otherwise predisposed to develop renal failure.¹⁰¹ The use of “renal-dose” dopamine has a controversial history marked by conflicting studies. A large randomized controlled trial in adults concluded that it did not confer clinically significant protection from renal dysfunction.¹⁰² Definitive studies on renal-dose dopamine are lacking in children. Fenoldopam, a selective dopaminergic agent and more potent renal vasodilator than dopamine, has shown some promise in preventing and treating acute renal failure in adults.^103,¹⁰⁴

Early institution of renal replacement therapy in the face of acute renal failure decreases morbidity.¹⁰⁵ Peritoneal dialysis is an excellent modality for infants and children, although trauma patients may have contraindications. Continuous venovenous hemofiltration dialysis is an excellent choice in a high-acuity or head-injured patient requiring a steady hyperosmolar state for control of ICP. It offers the benefit of constant and gentle manipulation and control of intravascular volume, electrolytes, dialyzable molecules, and serum osmolarity.¹⁰⁶ The development of regional anticoagulation with citrate-induced hypocalcemia has increased the efficacy and safety of continuous venovenous hemofiltration dialysis, especially in children at risk for bleeding from systemic anticoagulation.

Special Considerations

Imaging

Spinal Trauma

• Injuries in young children commonly involve C1, C2, and C3. In older children and adolescents, the injury pattern is similar to that in adults, predominantly involving the mid and lower spine.¹⁰⁷

• Recent evidence supports the use of selective criteria in imaging.^108,¹⁰⁹

• The lateral radiograph is the most important view, especially in children younger than 5 years. The false-negative rate for a single cross-table lateral view is 21% to 26%. For this reason, additional views and/or CT scan is indicated.¹⁰⁷ Practice guidelines, however, have changed, and CT has replaced plain radiography.¹⁰⁹ A recent paper concludes that “lateral view radiographs showed a borderline acceptable diagnostic sensitivity for the detection of traumatic cervical spine abnormalities compared with CT while the addition of other views did not seem to improve the diagnostic performance of conventional radiography.”¹¹⁰

• Considerations when interpreting lateral C-spine include:

1 Predental space up to 5 mm is normal.

2 Pseudosubluxation of C2 or C3 is a common pitfall on lateral radiographs of the cervical spine. A normal posterior cervical line does not exclude underlying ligamentous injury at C2-C3.¹⁰⁷

3 Above the glottis, soft-tissue thickness of 7 mm or more is considered abnormal; below the glottis, a measurement of 14 mm should be considered abnormal.¹¹¹

4 A distance of 6 mm or more between the lateral mass of C1 and the odontoid process is suggestive of ligamentous disruption of the transverse ligament.

5 Posterior tilting of the odontoid is a common normal finding; however, anterior tilting is abnormal and suggests injury.

6 When evaluating for atlanto-occipital dislocation, a gap of more than 5 mm between the occipital condyles and the condylar surface of the atlas is highly suggestive of craniocervical injury. A line drawn along the posterior aspect of the clivus toward the odontoid should intersect the odontoid.¹⁰⁷

7 Wedged C3 vertebral body is a normal phenomenon in infants and young children.

• Thoracic lumbar spinal injuries: the most common injury of the thoracolumbar spine is a flexion injury. This often results in anterior compression fractures. The more severe the injury, the greater the likelihood of posterior ligamentous injury. It is very important to look for abnormalities of the disc space, widening of the interspinous distance and neural foramina, and fractures of the spinous process and neural arch. Transverse fracture of the vertebral body with anterior or lateral dislocation of the upper half of the fractured vertebra is called a Chance fracture and is common in lapbelt injuries. Associated abdominal injuries, especially to the bowel, are common.

• MRI should be obtained when cord injury is evident or cannot be ruled out and to evaluate ligamentous injury. Some researchers, however, point out that MRI overreads ligamentous injuries.

• Contrast “blush” occurs in greater than 6% of patients,¹¹⁵ is not associated with a negative outcome, and can be treated without surgery.

Genitourinary Trauma

• CT findings of renal injury are as follows. For contusion: focal patchy enhancement or striated nephrogram. For laceration: irregular, linear, hypodense parenchymal abnormalities. For shattered kidney: multiple separated fragments, some of which may not enhance owing to a lack of perfusion. For subcapsular hematoma: superficial crescentic hypodense area compressing adjacent parenchyma. For segmental arterial injury: wedge-shaped perfusion defect. For devascularized kidney: diffuse lack of enhancement of kidney. For renal vein thrombosis: persistent nephrogram on delayed images and renal swelling.¹¹⁴ Delayed images are essential in the evaluation of renal trauma.

• Blunt trauma to the ureteropelvic junction is associated with transverse process fractures (30%).

• In infants and young children, a full bladder becomes an abdominal organ, as it arises out of the pelvis and is more prone to injury because it is not as protected as the adult urinary bladder.

• CT cystography is highly accurate as an adjunct to routine abdominopelvic CT in the trauma setting. It obviates the need for a separate study with conventional cystography, which entails additional cost and more radiation exposure.

Infectious Disease and Immunology

A child who sustains trauma is susceptible to infection in several ways. The trauma itself may destroy the barriers of skin and mucosa, allowing both pathogenic and nonpathogenic organisms the opportunity to establish a productive infection. In addition, significant immune dysfunction occurs following trauma; both nonspecific and specific abnormalities have been described in cellular and humoral responses, as well as in macrophage and neutrophil function.¹¹⁶^–¹¹⁸ More recent investigations provide data on cytokines and other mediators and molecular markers of inflammation, both circulating and cell surface.^119,¹²⁰ These abnormalities of immune dysfunction can be categorized under two basic mechanisms: hyperactive systemic proinflammatory processes and depression of cell-mediated immunity. Hyperactive proinflammatory responses may be ultimately deleterious to a child, leading to SIRS, multiple organ dysfunction syndrome, and death. Hyperactive proinflammatory response may be the result of priming the trauma patient for an exaggerated response to a second inflammatory stimulus, referred to as the two-hit hypothesis. Differences in the characteristics of immune dysfunction appear to be a function of the type of trauma (e.g., TBI, blunt trauma, burn injury) and appear to change over time after trauma to reflect changes in the acute activation seen immediately after the injury, with subsequent evolution into immune suppression.¹¹⁸ Many of the abnormalities may be directly correlated with the severity of injury.¹¹⁷ Infections occurring within approximately 5 to 7 days of admission are more likely to represent inoculation at the time of trauma, whereas infections occurring after the first week of trauma reflect nosocomial pathogens present in the trauma center.

Empirical antibiotic therapy of the pediatric trauma patient on admission to the ICU is not well studied. Extrapolation from prospective controlled surgical studies in adults has provided some support for empirical prophylactic therapy, with the selection of antibiotics designed to provide reasonable coverage against anticipated pathogens. However, each trauma case should be evaluated individually for the types of organisms likely to cause infection, with empirical antibiotic therapy tailored to the location and severity of injury. No published data exist on the benefits or risks of empirical therapy for fungi or multiply resistant environmental bacteria in soil-contaminated injuries; therefore, extremely broad-spectrum antibiotic and antifungal agent prophylaxis is usually not recommended. Cultures obtained at the time of admission and surgical closure of open wounds can help the trauma team evaluate the child for infection later in the hospital course. Tetanus immunization should be considered in a child with devitalized, ischemic, and denervated tissues that have been inoculated by soil, or with deep tissue injury by foreign objects that have been in contact with soil.

Nosocomial infections of indwelling vascular catheters, surgically implanted foreign bodies, the lung, the urinary tract, and injured tissues are all well recognized, with therapy targeted to the organisms prevalent in the ICU. Gram-stained exudates and cultures can assist in providing information on the types and susceptibilities of the nosocomial pathogens causing infection. Providing sufficiently broad coverage empirically to achieve a high likelihood of success may both improve patient outcomes and decrease the emergence of certain antibiotic-resistant organisms. The definitive selection of antibiotics and a decision on the duration of therapy should be based on the isolated or suspected pathogens and the child’s response to therapy. A poor response to broad-spectrum therapy despite the use of antimicrobial agents active against the isolated pathogens suggests either a hidden focus of infection, which may require further investigation and possible surgical intervention, or additional antibiotic-resistant pathogens not originally isolated. Lack of response to therapy may also be related to noninfectious causes of clinical instability. Therapy should not be continued indefinitely, because subsequent colonization and infection by antibiotic-resistant bacteria or yeast are likely to occur. Once antimicrobial therapy is discontinued, careful observation for relapse or recurrence of infection is essential.

Several therapies have been suggested to obviate the consequences of immune dysfunction in trauma patients. Circulating granulocyte colony-stimulating factor has been shown to be highest on postinjury day 1 and then quickly declines to near normal values by postinjury day 3.¹²¹ In addition, plasma from trauma patients suppresses bone marrow colony growth of granulocyte-monocyte precursors for up to 2 weeks after injury.¹²² Administration of filgrastim in neutropenic, septic, and head-injured patients has resulted in improved generation and function of neutrophils.¹²³ Prophylactic use in patients with TBI showed a dose-dependent decrease in the frequency of bacteremia.¹²⁴ Because there is a complex relationship between the neuroendocrine and immune systems, many studies have explored hormonal therapies to improve T-cell and macrophage function. Potential therapeutic agents after trauma include dehydroepiandrosterone and prolactin and metoclopramide. In addition, hypertonic saline may improve T-cell function and possibly prevent the exaggerated proinflammatory response leading to lung injury.

Coagulopathies

Trauma is a potent activator of the inflammatory response, and a growing body of literature describes the relationship among inflammatory cytokines, endothelial function, and coagulation through cellular and molecular signaling.¹²⁵ A severely injured child is at risk for impaired hemostasis as well as pathologic thrombosis.

Activation of the coagulation cascade is proportional to the stimulus. Local thrombus formation by a discrete injury is protective by inhibiting local bleeding, and pathologic thrombosis is normally impeded by anticoagulant mechanisms. Massive activation of the coagulation axis can overwhelm the counterbalancing mechanisms, leading to deep venous thrombosis locally or microvascular thrombosis systemically. The latter culminates in varying degrees of clotting factor consumption and pathologic and protective thrombolysis and may ultimately result in disseminated intravascular coagulopathy (DIC). The microangiopathic thrombosis of DIC can also contribute to hemolytic anemia, ARDS, and organ failure remote to the site of traumatic injury. The epidemiology of injuries in children puts them at increased risk for trauma-induced DIC because the brain and liver release strong procoagulant thromboplastins. Indeed, the likelihood of coagulopathy has an inverse relationship to the presenting GCS score.¹²⁶ A recent paper showed that in children who meet clinical criteria for a head CT scan after trauma, a low plasma D-dimer strongly suggests the absence of significant brain injury.¹²⁷

Evaluation and treatment of physiologic derangements that promote bleeding are necessary in an injured child. Although definitive evaluation by laboratory assays may not be available immediately, early suspicion of coagulopathy based on clinical history, physical examination, and medical interventions may be life saving in a traumatically injured child.

Even in the absence of a coagulopathy at presentation, it is necessary to prevent iatrogenic coagulation disturbances. Dilutional coagulopathy can occur with the administration of as little as one unwarmed blood volume. After one to two blood volumes, platelets can be halved, and the activated partial thromboplastin time and prothrombin time can be doubled. In an injured child receiving blood products, coagulation studies should be sent early. As volume resuscitation continues, these studies should be checked frequently to refine blood product administration. Hypothermia may contribute to coagulopathy during resuscitation and should be prevented.

If a patient has normal coagulation values but continues to bleed diffusely, an underlying bleeding diathesis should be considered. Von Willebrand disease is the most common congenital bleeding disorder and has traditionally been assessed by a bedside bleeding time. However, uncertainty about the sensitivity, reliability, and predictive value of the bleeding time has led to a decline in its use. A platelet function assay, PFA-100, has been compared with bleeding time and is considered a superior screening test for primary hemostasis disorders.¹²⁸ Thromboelastography is recommended to assess and treat the coagulation state of an actively bleeding trauma patient.¹²⁹

Recombinant factor VIIa has been recommended for controlling bleeding in blunt trauma patients. Several papers address its use in coagulopathic trauma patients requiring emergent craniotomy. It has been shown to reduce the size of intracranial hematomas and reduce need for transfusion with packed red blood cells (PRBC) and plasma.^130,¹³¹ A recent meta-analysis, however, demonstrated no improvement in functional outcome or survival.¹³² Thromboembolic complications have been reported in adults and children and need to be taken seriously.

Although the overall physiology of coagulation in children is nearly identical to that of adults, there are some special considerations in injured children. The neonate’s relatively immature liver and initial nutritional state increases the likelihood that vitamin K–dependent clotting factors will be decreased. Trauma resulting from abuse in infants and children frequently includes occult head injuries and the release of potent thromboplastins. Young children may have an undiagnosed congenital bleeding disorder. Compared with adults, the relative health of the cardiopulmonary and renal systems allows children to tolerate significant hypovolemia and large-volume resuscitation that may result in a dilutional coagulopathy. The medical disorders and medications that can promote bleeding in adults also apply to children, although most are far less prevalent in the pediatric population.

In the ICU, patients are at increased risk of pathologic thrombosis secondary to endothelial damage and indwelling central catheters. Traumatic and pharmacologic paralysis, in addition to bed rest, contributes to venous stasis. Although the risk of deep venous thrombosis and thromboembolic disease is lower in prepubertal children than in adults, it is more prevalent than previously recognized.^133,¹³⁴ Hypercoagulable states occur across the age spectrum, and children with nephrotic syndrome, inherited forms of thrombophilia, and some rheumatologic disorders are at increased risk for pathologic clot formation. Prophylaxis with low-dose heparin or automated venous compression stockings should be used in appropriate patients.

Nutrition

Nutritional support of critically injured children is extremely important and is based on knowledge gained from research in critically ill adult and pediatric patients, as well as physiologic differences between pediatric and adult patients. A key difference is the requirement for maintenance of growth and development. The resting basal metabolic rate of pediatric patients is approximately 50% higher than in adults. In addition, pediatric patients have lower energy stores than adults.

A state of hypermetabolism is well documented in adult patients after major traumatic injury and surgical stress. Similar data also exist in critically ill pediatric patients and pediatric trauma patients. Following an extensive review of the literature, the “Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents” lists as a treatment option the replacement of 130% to 160% of resting metabolism after TBI in pediatric patients.⁷⁴ Patients who are paralyzed or in barbiturate coma have a lower resting metabolic rate and require fewer calories.

The enteral route is preferable, and much research has been performed related to the benefits of enteral versus parenteral nutrition. In a meta-analysis, benefits of enteral nutrition included lower risk of infection and reduction in hospital length of stay.¹³⁵ Other proposed benefits include preservation of intestinal mucosal integrity, with decreased bacterial translocation and decrease in multiple organ failure. Enteral feeding is also more cost-effective than parenteral nutrition in pediatric patients.¹³⁶ There are many adult studies supporting initiation of enteral feeding within 24 to 72 hours of ICU admission. When enteral feeding is not possible, it is best to support the patient with total parenteral nutrition.

Owing to impaired GI motility in critically ill trauma patients, enteral feeding may be poorly tolerated. Gastric emptying is often delayed following severe head injury. In addition, many of the medications used during treatment of traumatically injured patients may affect GI motility. Narcotics, benzodiazepines, and catecholamines can adversely affect feeding tolerance. Barbiturates decrease GI motility, and severe gastroparesis has been described. Many patients with severe TBI requiring barbiturate coma do not tolerate full enteral nutrition.

Large gastric residual volume associated with lack of tolerance of gastric feeding may increase the incidence of aspiration pneumonia and has been associated with higher ICU mortality in adults.¹³⁷ Continuous gastric infusion of formula, addition of prokinetic agents, or transpyloric feeding may improve feeding tolerance. In some pediatric trauma patients, enteral feeding is unrealistic. The most important action is to provide nutritional support as soon as feasible, with the decision of enteral versus parenteral support individualized to the patient.

Two special topics deserve mention. First, although there are no data regarding the effect of immune-enhancing and immune-modulating nutrition in pediatric patients, in adults, supplementation of arginine, glutamine, branched-chain amino acids, nucleotides, nucleosides, and omega-3 fatty acids has been used to improve outcome.^138,¹³⁹ These special formulations show promise with respect to decreased length of stay and decreased infectious complications.¹⁴⁰^–¹⁴² Second, control of blood glucose levels in adult surgical ICU patients has been shown to have an important beneficial effect. Tight glucose control with insulin significantly reduced morbidity and mortality in these patients.¹⁴³ Tight glycemic control has been shown to decrease infection and improve survival in pediatric burn patients. Similar studies have not been performed in pediatric trauma patients.

Sedation and Pain

Injured children commonly require analgesia and anxiolysis during therapy and management of various injuries. There are myriad drugs that can be safely used to provide appropriate levels of analgesia and anxiolysis.

In addition to providing pain relief and anxiolysis, sedatives and analgesics may reduce elevated ICP, facilitate mechanical ventilation, prevent shivering, provide anticonvulsant activity, and minimize long-term psychological trauma from untreated pain and stress.⁷⁴ The importance of restoring and maintaining circulating intravascular volume before administering sedatives cannot be overstated, as children may be “surviving” on endogenous catecholamine release, thereby barely maintaining adequate blood pressure and tissue perfusion. Administration of even small doses of any sedative in this situation may precipitate cardiovascular collapse and cardiac arrest. Empirical treatment of presumed hypovolemia should precede administration of sedatives in an acutely injured child.

In the initial setting of evaluating an acutely injured child, small doses of narcotics such as fentanyl, given in incremental doses (0.5 µg/kg per dose, up to 1 to 2 µg/kg) titrated to effect, can be useful in both providing analgesia and allowing a more detailed examination. A child with painful injuries (e.g., fractures, multiple abrasions) is often more cooperative and allows a more thorough examination after receiving adequate analgesia. Concerns about “masking” the presence of intraabdominal injury are unfounded, as the cooperation achieved from the analgesia outweighs the difficulty in examining an agitated, screaming child who is experiencing acute pain. It is rarely necessary to administer benzodiazepines or other anxiolytic drugs in the acute setting of pediatric trauma, provided adequate analgesia is given. In a mechanically ventilated patient, benzodiazepine (midazolam, diazepam, lorazepam) administration by intermittent dosing or by continuous infusion is commonly used to provide anxiolysis. Recently, infusion of dexmedetomidine has been used for sedation.

A variety of short-acting drugs can be used to provide hypnosis and loss of consciousness for endotracheal intubation. A detailed analysis of the advantages and disadvantages of these drugs is beyond the scope of this chapter. It should be noted that there is an increased risk of adrenal insufficiency following etomidate exposure in critically injured patients.¹⁴⁴

Sodium thiopental (4-6 mg/kg) is commonly used in a hemodynamically stable child in this setting because it is rapid acting (30-60 seconds) and can be used to treat elevated ICP. Further, sodium thiopental (1-2 mg/kg every 15-30 minutes) can be used following successful intubation to maintain unconsciousness during transport to the ICU, operating room, or radiology department. The use of thiopental for sedation for radiographic procedures in a nonintubated, spontaneously breathing patient should be reserved for elective situations in fasted patients, and it should be administrated by an anesthesiologist.⁷⁴ Pentobarbital may be substituted for sodium thiopental.

Except for inducing general anesthesia, the use of propofol for critically injured children is controversial and in fact is rarely necessary in the acute setting. A poorly defined syndrome of metabolic acidosis and myocardial failure has been reported after giving propofol by continuous infusion in the critical care setting. Nevertheless, many pediatric intensivists use propofol for short intervals, especially during the weaning of narcotic-dependent children from mechanical ventilation.

Inflicted Trauma

Abuse is a common cause of traumatic injury in infants and young children.^145,¹⁴⁶ The American Academy of Pediatrics has recently recommended use of the term abusive head trauma (AHT) rather than the term shaken baby syndrome.¹⁴⁷ Nationally, it is estimated that 1756 children died due to abuse or neglect in 2007, a rate of 2.35 per 100,000 children. Children younger than 12 months accounted for 43.7% of these fatalities, and 85% were younger than 4 years. Recognition of inflicted injury is important to ensure appropriate care, prevent recurrence of abuse, protect siblings, and comply with reporting mandates.

A delay in seeking care is common in children with abusive injuries. Injury history may be absent, incomplete, or inconsistent with physical findings or the developmental capability of the child. Domestic violence is common in families of abused children. Children with inflicted injuries that have more subtle findings and patients with intact families are more likely to be misdiagnosed as accidentally injured. This may have serious repercussions, including further injury and death.¹⁴⁸ Children with abusive injuries have worse outcomes than those with accidental injuries, with higher severity and mortality rates and higher patient costs.¹⁴⁹ Having a high index of suspicion for inflicted trauma is critical in assessing an infant that presents with lethargy, apnea, cyanosis, mottling, poor perfusion, or seizures without an obvious history of trauma.

Evaluation of children with inflicted injury should reflect the occult nature of many abusive injuries. The constellation of subdural hematoma, traction-type metaphyseal (bucket-handle) fractures of long bones, posterior rib fractures, and retinal hemorrhages are characteristic of inflicted injuries in infants. Although TBI is the leading cause of morbidity and mortality in abused children, some head injuries may not be easily diagnosed clinically.¹⁵⁰ Therefore, a nonambulatory infant with any type of abusive injury should have CT or MRI studies of the brain performed. The sudden deceleration with forceful striking of the head against a surface is an important mechanism responsible for inflicted brain injuries in children. Hypoxic-ischemic insults and other mechanisms also appear to play a role. Subdural hemorrhage, classically localized at the parieto-occipital convexity or posterior interhemispheric fissure, is the most consistent autopsy finding in shaking-impact syndrome. Subdural hematoma results from rotational deceleration forces that cause shearing of bridging cortical veins. Retinal hemorrhages are present in the majority of children with inflicted injuries, but their absence does not rule out abuse. In addition, not all retinal hemorrhages are due to abuse. Infrequently, accidental head injuries may cause retinal hemorrhages.^151,¹⁵² Therefore, an evaluation by a pediatric ophthalmologist is recommended in all children with suspected AHT. A skeletal survey should be done in all children with serious injury due to abuse. Screening for abdominal trauma is also important, either through imaging or laboratory studies. A psychosocial evaluation is critical in families of children with inflicted injuries. This is to help support the family during a time of crisis; evaluate for other comorbid factors such as domestic violence, substance abuse, and mental illness; comply with mandated reporting requirements; and help interface with investigative and protective agencies.

A multidisciplinary team is optimal for treating children with inflicted injuries. The team should consist of the treating staff, a medical social worker, and a child abuse pediatrician.

Rehabilitation

Once life-threatening conditions have been ameliorated and the medical condition stabilized, the pediatric trauma patient should be assessed for the restoration of maximal functional independence. It is the role of the pediatric physiatrist and rehabilitation medicine team to identify, assess, and promote maximum restoration of physical, cognitive, and psychosocial functioning in each patient. Recently, amantadine has been used to facilitate recovery of consciousness in children with acquired brain injury; while on amantadine, physicians noted improvements in consciousness.¹⁵³ Members of the rehabilitation team, including occupational therapists, physical therapists, speech therapists, social workers, and schoolteachers, provide their expertise in returning the patient to maximum independent function. As a first step, it is important to identify the patient’s functional deficits and subsequent level of disability and handicap as they relate to the patient’s home, community, and school settings.

The rehabilitation process should begin early in the patient’s critical care stay, because physical and occupational modalities may limit the adverse physiologic effects of prolonged immobilization. For instance, muscles lose their flexibility and bulk, resulting in diminished strength and endurance. Joints become stiff and contracted, and skin breaks down, creating pressure ulcers. Interventions include passive joint range of motion, isometric strengthening, and appropriate bed positioning. Orthotic devices, placed at joints (e.g., elbows and ankles) in a neutral position, limit contracture formation. Speech and occupational therapists can evaluate oral motor function to assess safe swallowing and feeding, decreasing the patient’s risk of aspiration. The dietitian evaluates the patient’s nutritional status, providing recommendations for appropriate diet and caloric intake. The social worker and child life specialist provide the patient and family members with emotional and educational support during the patient’s acute critical care stabilization.

It is through the collaborative efforts of the pediatric trauma team and the pediatric rehabilitation team that the survivor of a pediatric trauma maximizes functional independence and has a successful discharge home.

Brain Death and Organ Donation

The first definition of irreversible coma as a criterion for death, as well as the criteria for diagnosis, was published in 1968 by an ad hoc committee of the Harvard Medical School. In 1981, the President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research published a report titled “Defining Death: Medical, Legal, and Ethical Issues in the Determination of Death,” which summarized medical practice for the determination of cardiorespiratory and neurologic death. A summary of the guidelines was published in the medical literature. These guidelines provided a conceptual definition of brain death and left the criteria for determination up to accepted medical standards. In addition, it established common ground for law related to the diagnosis of brain death. In 1987, the American Academy of Pediatrics published guidelines for the determination of brain death in pediatric patients,¹⁵⁴ with specifications for physical examination, observation period, and confirmatory laboratory testing. These guidelines have attempted to define the clinical determination of irreversible cessation of all brain function to the best of medical ability. The need to define brain death was fueled by improvements in the intensive care of critically ill patients, as well as advances in solid-organ transplantation. There is continued debate by experts regarding whether patients who have been determined to be brain dead by current guidelines have irreversible loss of all brain function. In addition, controversy exists regarding whether brain death should be defined as loss of higher brain function and not loss of all brain function.¹⁵⁵

Trauma patients represent a large percentage of those who are declared brain dead in a pediatric ICU and therefore a large pool of potential organ donors. There continues to be a wide gap between the number of organs available for transplantation and the number of patients needing transplants, with more than 100,000 patients currently awaiting transplantation in the United States. Improvement in consent for organ donation is one way to decrease this gap. Despite widespread acceptance of and support for organ donation among the general public, only 40% to 60% of families give consent for donation. Consent rates for donation are improved when the family understands the concept of brain death and when the understanding occurs before the request for donation (decoupling). In addition, the consent rate is maximized when the requester has specialized training or is a member of the organ procurement organization. In pediatric trauma patients, involvement of the attending physician in the request process may also have a beneficial effect on consent rates.¹⁵⁶

In an effort to increase organ donation, federal regulations were issued in 1998 governing how potential organ donors should be identified and approached.¹⁵⁷ All hospitals must have an agreement with an organ procurement organization (OPO) and must notify the organization of patient deaths. The procurement organization then determines the patient’s suitability for organ donation. In addition, the hospital must have an agreement with a tissue bank and eye bank to coordinate tissue and eye donation. The family of every potential donor must be informed of the option to donate organs or tissues.

Until recently, virtually all organ donors were declared brain dead before organ procurement. In the early 1990s, the University of Pittsburgh introduced a protocol for non-heartbeating cadaveric donation. This policy has increased the pool of available organs and has generally resulted in satisfactory results.^158,¹⁵⁹ There is controversy in the medical community regarding the ethics of these protocols.^160,¹⁶¹ Part of this controversy revolves around the dead donor rule. Some physicians have requested a moratorium on non-heartbeating donation pending further ethical discussion and analysis.

Victims of child abuse represent a special subset of pediatric patients. The documentation of injuries in child abuse cases is extremely important and has significant legal ramifications. The medical examiner plays a key role in determining whether legally deceased child abuse victims may be released for organ procurement. The medical examiner may prohibit organ procurement if there is concern that the process will alter forensic evidence. Implementation of procedures to fully document the state of the abdominal cavity and the extent of abdominal injuries in the operating room before procurement may facilitate release for donation.

Documentation may be performed by the transplant surgeon or the medical examiner.^162,¹⁶³