Paul I. Reynolds,Oliver Soldes,
Shobha Malviya,
Peter J. Davis
|
|
Trauma Centers and Classification, 991 |
||||||||||||||||||||||
|
|
Trauma Resuscitation, Diagnosis, and Prioritization, 991
|
||||||||||||||||||||||
|
|
Specific Injuries, 998
|
||||||||||||||||||||||
|
|
Perioperative Management, 1006
|
||||||||||||||||||||||
|
|
Summary, 1010 |
Childhood injuries are a major public health problem. Trauma is the number one killer of Americans aged 1 to 19 years, causing more than 16,000 deaths in 1999 in the United States. More than 60% of the deaths in this age group are related to injuries ( Anderson, 2001 ), with traumatic brain injury (TBI) being the leading cause of death (70%) and long-term disability. Thoracic and abdominal injuries are the cause of death in 20% and 10% of trauma fatalities, respectively ( Cooper et al., 1994 ).
Pediatric trauma remains a surgical disease, despite the large numbers of minor childhood injuries and successes in the nonoperative management of many solid organ injuries. Nonoperative management is more widely used in the pediatric trauma population than in adults. Operative management of solid organ injuries is required when hemodynamic instability or severe physiologic compromise develops. Data from an analysis of the National Pediatric Trauma Registry (NPTR) demonstrate that more than half of injured children have a diagnosis that requires evaluation by a surgeon and 11% require an operative procedure. Tepas and others (2003) reported that 32% of children in their study sample were considered at potential risk of death from their injuries. Of these, 86% had injuries requiring surgical evaluation, 21% required an operative procedure, and 12% died.
With careful assessment and continuing reassessment, many blunt head, chest, and abdominal injuries can be managed nonoperatively. The decision to pursue nonoperative therapy should be made by the surgical specialist caring for the patient. The periodic failure of nonoperative management requires rapid recognition and a decision to perform an urgent operation.
Trauma injuries can be broadly divided into (1) blunt and penetrating trauma and (2) burns. Blunt trauma is considerably more difficult to evaluate than penetrating trauma and relies more heavily on imaging studies. Nonburn traumatic injuries in children are approximately 90% blunt and 10% penetrating ( Potola et al., 2000) ; urban centers may have a higher proportion of penetrating trauma. Thermal and chemical burn injuries are discussed in Chapter 29 , Anesthesia for Children with Burns.
▪ TRAUMA CENTERS AND CLASSIFICATION
Death from pediatric trauma occurs at three periods: (1) within seconds of the traumatic event due to overwhelming injuries; (2) within minutes to hours of the event (the “golden hour”), when aggressive intervention with attention to the ABCs (airway, breathing, and circulation) can make a difference in survival ( Roback, 2000 ); and (3) days to weeks after the initial event when complications such as organ failure, sepsis, or brain death arise. An effective way to minimize morbidity and mortality due to trauma arose from lessons learned in the management of injured men and women during the Korean Conflict and Vietnam War ( Morrison, 2002) . During the past several decades, the American College of Surgeons and other organizations developed a three-tiered system for trauma center designation and verification ( Table 30-1 ). Level I centers offer the widest range of services for the most severely injured patient, whereas level III centers allow for stabilization and triage. Because 25% of all trauma occurs in children, specific systems of pediatric trauma care developed within the adult systems. The first pediatric-specific trauma centers were developed in the early 1970s in Boston, Ann Arbor, Baltimore, Washington, DC, Toronto, and Brooklyn ( Morrison et al., 2002 ). Since that time, more than 15 level I and level II pediatric trauma centers have been certified by the American College of Surgeons.
TABLE 30-1 -- American College of Surgeons trauma center levels and descriptions
|
Level I |
|
Provides comprehensive trauma care, serves as a regional resource, and provides leadership in education, research, and system planning. |
|
Level II |
|
Provides comprehensive trauma care either as a supplement to a level I trauma center in a large urban area or as the lead hospital in a less population-dense area. |
|
Level III |
|
Level III facilities typically serve communities that do not have immediate |
From MacKenzie EJ, et al.: National inventory of hospital trauma centers. JAMA 289:1516, 2003. © 2003 American Medical Association.
Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com
Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.
Copyright © 2005 Mosby, An Imprint of Elsevier
▪ TRAUMA RESUSCITATION, DIAGNOSIS, AND PRIORITIZATION
The initial phase of the acute care of the trauma patient is resuscitation. This dynamic and crucial period involves continuous assessment with concurrent diagnostic and therapeutic procedures to preserve life and prevent morbidity ( Rhodes, 1998 ). The Advanced Trauma Life Support (ATLS) course of the American College of Surgeons provides the basis of a systematic protocol to guide initial resuscitation and evaluation of the trauma patient and is summarized later ( American College of Surgeons Committee on Trauma, 1997 ). The care of a trauma patient is divided into several phases: primary survey with concurrent resuscitation, secondary survey, and definitive care. Trauma patients require continuous reassessment for missed injuries and changes in known injuries.
▪ PRIMARY SURVEY WITH CONCURRENT RESUSCITATION
According to basic and advanced pediatric life support guidelines, the primary survey is a rapid evaluation and treatment phase focusing on the “ABCDEs”:
|
|
Airway: Ensure a patent airway. |
|
|
|
Breathing: Assess and provide adequate respiration. |
|
|
|
Circulation: Assess and assist the circulation with intravenous fluids and cardiopulmonary resuscitation (CPR) as needed. |
|
|
|
Disability: Assess the neurologic injury. |
|
|
|
Expose: Remove clothing to assess and evaluate for further injury and then take appropriate steps to prevent hypothermia. |
The secondary survey is composed of a complete physical examination, patient history, laboratory tests, and radiologic imaging. This phase may be delayed or completed in the operating room in patients who require urgent interventions. Definitive care occurs in the intensive care unit and/or operating room and often involves care by pediatric surgical subspecialists (neurosurgeons, orthopedic surgeons). Patients may also require transfer to comprehensive trauma centers during this phase ( Krantz, 1996 ). During the primary and secondary stage of evaluation, patients may be categorized using a grading system based on acuity and severity of their trauma. A pediatric trauma classification system is outlined in Table 30-2 . In addition, Figure 30-1 illustrates guidelines for airway and cardiovascular assessment in the traumatized pediatric patient.
TABLE 30-2 -- University of Michigan pediatric trauma classification
|
Level 1 |
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
Pediatric Patients with Single or Multisystem Injuries and Unstable Vital Signs with One or More of the Following |
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
Level 2 |
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
Pediatric Patients with Multisystem Injuries and Stable Vital Signs |
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
Level 3 (“trauma consult”) |
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
Pediatric Patients who are Conscious with an Apparent Isolated Injury and Stable Vital Signs with a Mechanism of Injury with a Low Potential for Multisystem Injuries |
|||||||||||||||||||||||||||||||||||||||||||||||||||
|
|
FIGURE 30-1 Guidelines for airway and cardiovascular assessment in the traumatized pediatric patient. |
▪ AIRWAY AND BREATHING
The first step in trauma resuscitation is securing an airway and ensuring adequate respirations. Indications for endotracheal intubation include oxygenation and ventilation, and protection of the airway against aspiration. Appropriate management of the airway may be challenging or difficult without proper preparation and familiarity with the unique characteristics of the pediatric airway. In a young child or infant, the tongue is relatively large and the larynx and glottic opening are more anterior. The most obvious differences are that the child's airway has a smaller diameter and a shorter length. Airway edema occurring in an already small airway results in significant changes in the internal diameter of the airway and in increased resistance to airflow. The short length of the trachea makes right mainstem intubations more likely and increases the likelihood of extubation from small positional changes of the endotracheal tube. The narrowest anatomic portion of the pediatric airway is at the cricoid cartilage throughout childhood, unless the glottis is partially or completely closed.
The initial management of the pediatric airway involves bag-valve-mask ventilation with a jaw-thrust maneuver and an Ambu bag. Intubation is indicated in patients with respiratory or cardiac compromise or an altered level of consciousness. Endotracheal intubation is the preferred definitive airway. Nasotracheal intubation may be suboptimal and difficult because of the small size and acute angle of the nasopharynx and the more anterior and cephalad position of the glottic opening. A laryngeal mask airway (LMA) may be used temporarily by persons familiar with their use but less skilled in intubation. However, it must be recognized that the LMA does not protect the airway from aspiration and must be replaced by an endotracheal tube as soon as skilled personnel become available. Endotracheal intubation of pediatric trauma patients in emergency situations is associated with a 25% rate of complications, such as bronchial intubation ( Nakayama et al., 1990 ).
The head and neck must be protected from unnecessary movement. The physician managing the airway (positioned at the head of the patient) must maintain the head and neck in anatomic alignment with the body. Forceful axial traction may cause further disruption of an unstable spine and must be avoided. In an unconscious, head-injured child, endotracheal intubation will protect the airway and provide ventilatory support. When endotracheal intubation is required before a radiograph of the cervical spine (C-spine) has been obtained, a spinal injury should always be assumed ( American College of Surgeons Committee on Trauma, 1997 ). Children are more likely—because of their neck musculature, their disproportionately large head size, and the elasticity of their supporting structures—to sustain cervical neck injuries above C3. It is frequently difficult to rule out a spinal cord injury because 50% of these injuries exist in the absence of radiographic findings.
Intubation of the child with a cervical neck injury requires keeping the patient supine and the neck in a neutral position and avoiding any head-tilt and or chin-lift maneuvers. While intubating patients with actual or presumed C-spine injuries, an assistant must apply manual inline axial stabilization—that is, the assistant holds a hand over each ear while keeping the patient's shoulders and occiput firmly on a rigid backboard ( Fig. 30-2 ). Intubation techniques involving rapid sequence, the use of the Bullard laryngoscope, flexible fiberoptic bronchoscopy, and techniques involving the use of fluoroscopy have all been described for patients with presumed C-spine injuries ( Watts et al., 1997 ; Criswell et al., 1994 ; Morell et al., 1997 ; Zanette et al., 1997 ) (see Chapter 10 , Induction of Anesthesia). Hastings and Wood (1994) have shown that in patients without head or neck stabilization, exposure of the arytenoid cartilage and best view of the glottis were achieved with 10 and 15 degrees of head extension, respectively. Head immobilization reduces the extension angles to 4 degrees for arytenoid exposure and 5 degrees for the best view of the glottis.
|
FIGURE 30-2 Manual axial inline stabilization during direct laryngoscopy. |
Short-acting sedatives to facilitate intubation are preferred in head-injured patients to allow reexamination. A quick and focused neurologic assessment should be performed before administering sedatives or paralytics, when medically safe. Children commonly develop gastric distention because of crying or bag-and-mask positive-pressure ventilation. A distended stomach may compromise ventilation and increase the risk of aspiration ( Fig. 30-3 ). The stomach should be decompressed with a nasogastric or an orogastric tube after intubation and a chest radiograph obtained to verify endotracheal tube position.
|
FIGURE 30-3 Gastric dilation frequently occurs after crying or positive-pressure ventilation by gas and mask. |
Depending on the nature of the underlying injury, securing the airway in a patient who has sustained multiple injuries or even isolated facial injuries can be extremely complicated ( Melillo et al., 2001 ) (Fig. 30-4 ). The management of such cases calls upon the resourcefulness and skills of the anesthesiologist and requires careful consideration of damage to surrounding structures such as major blood vessels and the airway structures themselves, the ability to maintain a patent airway via facemask, and the potential for an expanding hematoma that may subsequently compromise an airway that may be patent at the current time. Additional considerations include the risks of increased intracranial pressure (ICP) in the case of concomitant head trauma, of exacerbating an existing C-spine injury, and of aspiration during airway manipulation. The presence of rhinorrhea, otorrhea, or ecchymoses around the eyes should raise suspicion about a possible basilar skull fracture, and any instrumentation of the nasal passages, including passage of an endotracheal tube or a nasogastric tube, should be avoided. Similarly, crepitus at the neck may herald the presence of a tracheal or bronchial disruption, and intubation under direct vision using a flexible fiberoptic scope in a spontaneously breathing patient should be considered to avoid false passage of the endotracheal tube.
|
FIGURE 30-4 An 11-year-old girl fell 10 to 15 feet while sliding down the school banisters onto a plant supported by a thick wooden pole. She eventually was intubated orally with direct laryngoscopy. (From Melillo EP, Hawkins DJ, Lynch L, MacNamara A: Difficult airway management of a child impaled through the neck. Paediatr Anaesth 11:615-617, 2001.) |
In cases where airway difficulty is anticipated, it may be prudent to transport the child to the operating room with an anesthesiologist and otolaryngologist in attendance once the child has been stabilized hemodynamically and additional injuries have been ruled out. The airway may then be secured with preparations to perform an emergent tracheostomy in case of failure to intubate the trachea via direct laryngoscopy. A careful induction of anesthesia via the inhaled route may be tolerated by the patient who has received adequate volume resuscitation and permits direct laryngoscopy while the patient is breathing spontaneously. The use of muscle relaxants is best avoided until the airway is secured. If intravenous agents are required to induce anesthesia, it is preferable to use short-acting agents such as propofol and remifentanil. These agents effectively blunt ICP responses to direct laryngoscopy and allow for spontaneous respiration to occur in case of a failed intubation. The use of a combined propofol and remifentanil technique provides an alternative to a traditional rapid sequence induction ( Haughton et al., 1999 ).
Ensuring adequate ventilation is the next task after securing the airway. Breathing is best assessed by auscultation and observation of chest motion. Young children in respiratory distress may exhibit subcostal and intercostal retractions. Nasal flaring and grunting also signal breathing difficulty. Assessment of tracheal position and jugular venous distention (for possible pneumothorax and cardiac tamponade) may be difficult because of the child's short, fat neck. Pallor, cyanosis, and an altered level of consciousness are late signs of respiratory insufficiency and demand immediate intervention. End-tidal CO2 monitoring, pulse oximetry, and blood gas determinations are useful adjuncts. Many injuries that impair respiration include simple tension and open pneumothorax, massive hemothorax, flail chest, and pulmonary contusion.
▪ CIRCULATION
Children who sustain multiple injuries frequently present in hypovolemic or hemorrhagic shock that must be promptly recognized and treated. Unlike adults, children maintain an almost normal blood pressure until 25% to 35% of their circulating blood volume is lost ( Fig. 30-5 ). This is likely due to their high sympathetic tone that causes peripheral vasoconstriction in an effort to maintain blood pressure in the face of a diminished blood volume. Tachycardia is an earlier sign of impending shock than is hypotension. Tachycardia generally indicates a loss of at least 10% of the patient's blood volume. In addition, signs of poor peripheral perfusion such as delayed capillary refill (>2 seconds), weak or thready pulses, mottling or cyanosis of the skin, and impaired consciousness are earlier indicators of shock than low blood pressure. The presence of hypotension as a result of hypovolemia should be considered an ominous sign that usually heralds impending cardiovascular collapse. In children, hypotension as a result of hemorrhage corresponds to a loss of approximately 25% of the blood volume, or 20 mL/kg ( American College of Surgeons Committee on Trauma, 1997 ). Bradycardia is a dangerous sign that indicates hypoxemia, impending arrest, or increased ICP. Table 30-3 describes the stages of pediatric shock and clinical signs seen at these stages.
|
FIGURE 30-5 Increase in systemic vascular resistance in response to hypovolemia preserves blood pressure until 25% of blood volume is lost. Hypotension is a late sign of hypovolemia. (From Rasmussen GE, Grandes CM: Blood, fluids, and electrolytes in the pediatric trauma patient. Int Anesthesiol Clin 32:79-101, 1994.) |
TABLE 30-3 -- Stages of pediatric blood volume loss (shock) and associated clinical signs
|
Blood Volume Loss |
|
Clinical Signs |
|
<20% |
CV: |
Tachycardia; weak, thready pulses |
|
|
Skin: |
Cool to touch, capillary refill 2 to 3 seconds |
|
|
Renal: |
Slight decrease in urine output, increase in specific gravity |
|
|
CNS: |
Irritable, may be combative |
|
25% |
CV: |
Tachycardia; weak, thready distal pulses |
|
|
Skin: |
Cold extremities, cyanosis and mottling |
|
|
Renal: |
Decrease in urine output |
|
|
CNS: |
Confusion, lethargy |
|
40% |
CV: |
Frank hypotension; tachycardia may progress to bradycardia |
|
|
Skin: |
Pale, cold |
|
|
Renal: |
No urine output |
|
|
CNS: |
Comatose |
It is imperative to rapidly assess the pediatric trauma patient for signs of shock on arrival at the emergency department and at frequent intervals thereafter. The initial fluid bolus administered in the trauma setting should be warmed isotonic crystalloid (lactated Ringer's or normal saline) in an intravenous bolus of 20 mL/kg. The pulse, capillary refill, and blood pressure should then be reassessed. A second bolus of 20 mL/kg should be administered if there is no significant response or only a transient improvement in these parameters. A third crystalloid bolus may be given, if necessary, to maintain appropriate vital signs and circulation. Then 10 mL/kg of blood should be administered next if additional fluid resuscitation is required. The need for blood transfusion initially is uncommon and usually signals “surgical bleeding” that may require operation.
If shock persists and fails to respond to fluid therapy, other causes should be sought. Such causes may include long bone or pelvic fractures. Pericardial effusion and tamponade are less common occurrences in blunt trauma than are penetrating injuries. The classic clinical signs of cardiac tamponade are shock, muffled heart sounds, and distended neck veins. Treatment requires immediate pericardiocentesis.
Pneumothorax is a common complication of blunt chest injury in children, with nearly one fourth under tension ( Nakayama et al., 1989 ). Unilateral or bilateral tension pneumothoraces may produce hypotension and hypoxemia. The classic signs of tension pneumothorax are ipsilateral tympany, shift of the trachea to the contralateral side, and distended neck veins.
Significant occult blood loss may be overlooked on the initial examination of the small child and infant. Because the absolute blood volume of a child is small, the significance of external blood loss may be underestimated. In addition, blood accumulation in the infant's large, expandable head, and open fontanels can produce shock. Careful assessment of the abdomen is central to evaluation of the injured patient in shock.
▪ VASCULAR ACCESS
Adequate large-bore intravenous access must be established as early as possible in the course of the resuscitation. Although peripheral routes offer the most rapidly accessible sites, such access may be difficult or impossible to obtain in the child with depleted intravascular volume or shock and resultant peripheral vasoconstriction. In such cases, a central venous catheter may be placed in the femoral vein if personnel with the necessary skills are available. Central venous catheters (specifically of the internal jugular or subclavian vein) are not recommended as a primary intravascular route during initial resuscitation because of the risk of pneumothorax or hemothorax during their insertion. Placement of these catheters is difficult in small children and infants under the best of circumstances, and C-spine immobilization precludes the appropriate neck position required for safe technique. Delays in establishing vascular access may be life threatening. Therefore, if these routes fail, intraosseous access should be rapidly initiated to expedite the administration of volume expanders and necessary pharmacologic agents. Once the child has been resuscitated, additional catheters should be placed.
Intraosseous access is placed in the medial surface of the proximal tibia 1 to 3 cm below the tibial tuberosity or the distal femoral metaphysis and has been used as a life-saving measure to establish short-term vascular access in critically ill or injured children ( Figs. 30-6 and 33-2 ). In a review of the use of intraosseous access in pediatric trauma patients under 10 years of age, Guy and others (1993) reported successful placement in 28 of 32 attempts. In this study, intraosseous access was established successfully by paramedics, nurses, and physicians. There were no long-term complications in the survivors, and there was one minor incident involving extravasation of fluid. The most common complication of intraosseous access is subperiosteal infiltration, which generally resolves spontaneously without further problems. Intraosseous access has a low complication rate; osteomyelitis and cellulitis occur in 0.6% and 0.7%, respectively ( Rosetti et al., 1985 ; Fiser, 1990 ). Other rare complications include fractures and emboli. Although very few complications have been reported with this technique, it must be recognized that the high mortality in patients who require intraosseous access prevents assessment of long-term complications.
|
FIGURE 30-6 Appropriate placement of the intraosseous infusion needle on the medial surface, distal to tibial tuberosity. (From Ellemunter H: Arch Dis Child Fetal Neonatal Ed 80:74F, 1999.) |
▪ DISABILITY AND DIAGNOSTIC EVALUATION
The diagnostic evaluation of the injured child involves clinical examination supplemented by radiologic examinations and laboratory testing. Imaging plays a major role in the evaluation of the injured child ( Vane, 2002 ). Improvements in imaging techniques have allowed progress in nonoperative management of abdominal and thoracic trauma, supplanting exploratory laparotomy and diagnostic peritoneal lavage (DPL) in many hemodynamically stable patients.
Initial plain film screening examinations in injured children who have mechanisms of injury compatible with serious injuries are generally limited to chest, pelvis, and lateral C-spine radiographs obtained in the emergency department trauma bay. Further radiographs are directed by physical findings (e.g., extremity deformity, spine tenderness). Spine films are obtained when spine tenderness, deformity, neurologic deficits, or inadequate examination in a patient prevents clinical spine clearance ( Fig. 30-7 ).
|
FIGURE 30-7 Lateral cervical spine radiograph of a 9-year-old involved in an automobile accident. Arrow points to an occipitoatloid (C1) dislocation. The patient died. |
Computed tomography (CT) is widely used in the evaluation of pediatric trauma. Head CT scans are routinely obtained in children with a history of loss of consciousness, altered mental status, and focal neurologic deficits. Neck CT is obtained to supplement cervical radiographic studies or when a C-spine injury may exist on the basis of clinical signs and symptoms. Whenever C-spine injuries may exist based on clinical judgment or the mechanism of injury, C-spine precautions and immobilization should be maintained. C-spine clearance in the brain-injured patient may not be possible until the patient's mental status has improved.
CT of the abdomen and pelvis is routinely used in the evaluation of abdominal injuries and tenderness or as a screening tool in obtunded patients ( Haftel et al., 1988 ; Vane et al., 2002) . CT scans are invaluable for the evaluation of injuries to solid organs or retroperitoneum. They are useful but less sensitive and specific for evaluation of hollow viscous injuries or intestinal perforation ( Bulas et al., 1989). CT scanning has largely replaced DPL in the initial evaluation of blunt pediatric abdominal trauma, although DPL may be a useful adjunct in selected patients. Focused abdominal sonogram for trauma (FAST) is of more limited value in the pediatric trauma population because many solid organ injuries produce minimal free fluid (lesser grades of spleen, liver, and kidney injuries) such that it may not be detected ( Coley et al., 2000 ).
As most pediatric trauma patients are generally healthy before their injury and take few or no medications, screening laboratory examinations are limited and focused. Children with minor injuries (e.g., upper extremity fractures) may undergo no or very limited laboratory testing. In more seriously injured patients, laboratory testing may generally be safely limited to specific clinical indications, rather than a generalized routine “trauma panel” ( Chu et al., 1996 ). A complete blood count, blood gas, blood typing and screening, and urinalysis are suggested for initial testing in seriously injured patients. Routine testing of liver functions, pancreatic enzymes, and coagulation parameters is of limited value and should be obtained only when clinically indicated.
▪ DISABILITY (NEUROLOGIC ASSESSMENT)
A brief rapid neurologic evaluation is performed as part of the primary survey. It should include assessment of the patient's level of consciousness and pupillary function. The AVPU method (Alert, responds to Voice, responds only to Pain, Unresponsive to stimuli) or the more detailed Glasgow Coma Scale (GCS) should be used. If AVPU is selected, the GCS calculation is performed during the secondary survey with a detailed neurologic examination. Periodic reassessment of the level of consciousness is necessary to detect neurologic deterioration due to progression of TBI, hypoxemia, or hypovolemia. Changes in mental status require prompt reevaluation of the ABCs. If the ABCs are adequately managed, then deterioration in mental status should be considered as due to TBI, prompting further brain imaging and consultation with a neurosurgeon.
▪ EXPOSURE
Exposure involves removing the trauma patient's garments, usually with shears, to allow detailed physical examination and detect injuries. Rolling the patient, while maintaining C-spine precautions, is necessary to identify injuries to the dorsal surface of the body that would otherwise be occult. Padding should be placed on the backboard at this time to prevent decubitus ulcer formation. This assessment should be rapid and the patient covered in warmed blankets and/or with a warming device to prevent hypothermia. In addition, intravenous fluids should be warmed and the room temperature raised. This is especially important in small children who are more prone to hypothermia due to their larger ratio of surface area to volume.
Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com
Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.
Copyright © 2005 Mosby, An Imprint of Elsevier
▪ SPECIFIC INJURIES
▪ FACIAL TRAUMA
Although severe facial trauma in children is a relatively uncommon event ( Zerfowski and Bremerich, 1998 ), when it does occur, it can make endotracheal intubation challenging, if not impossible ( Fig. 30-8 ; also see Fig. 30-4 ). Blood, secretions, hematomas, damaged tissues, and dentition may all obstruct the airway during respiration, ventilation, direct laryngoscopy, and fiberoptic intubation. Facial injuries can be categorized (in order of decreasing frequency) as soft tissue injuries, dental injuries, and facial fractures. As depicted in Figure 30-9 , the frequency of these injuries varies with the age of the child. In all instances, injuries are more common in males than in females. Facial trauma in children under 5 years of age is less severe because of the protective environment under parental supervision (Kaban, 1993 ). However, Shaikh and Worrall (2002) found that 42% of the pediatric population they sampled with facial injuries were younger than 5 years, with soft tissue injuries more common. The vast majority of these injuries were caused by falls, due to insecurities in motion and lack of coordination preventing victims from shielding their face or turning their head. The injury is then focused on a relatively small area of the face, from the nose to the mentum, referred to as “the falling zone” ( Zerfowski and Bremerich, 1998 ). Rates of soft tissue injuries rise again in adolescence, possibly explained by more aggressive, risky behavior, which may be related to alcohol consumption or sporting activities.
|
FIGURE 30-8 Protruding objects in the neck should never be pulled out because major vascular structures may be involved. In addition, hypertension during intubation must be avoided, as well as “awake” intubation. |
|
FIGURE 30-9 Type of injuries per year of age, demonstrated separately for soft tissue injuries, dental trauma, and fractures. (From Ferfowski M, Bremerich A: Facial trauma in children and adolescents. Clin Oral Invest 2:120-124, 1998.) |
Dental injuries occur at a lesser rate throughout childhood (compared with soft tissue injuries). Accidental aspiration of teeth before or during resuscitation can complicate care and necessitate removal via bronchoscopy. The least common form of pediatric facial trauma, accounting for only 8% of patients in the study by Zerfowski and Bremerich (1998) , was facial fractures. Nasal fractures are the most common facial fractures in children, accounting for more than 50% of all facial fractures in one study, followed by mandibular fractures and, last, maxillary fractures.
Another form of pediatric facial injury that can pose a challenge to anesthesiologists is oropharyngeal lacerations or impalement. It is not uncommon for children to fall with foreign objects in their mouths (e.g., pencil, toothbrush, etc.), sometimes sustaining abrasions or lacerations to the soft palate or oropharynx. Most are mild and spontaneously heal without intervention ( Hellmann et al., 1993 ). However, children require surgical extraction of the foreign body ( Fig. 30-10 ). In these instances, before extraction of a foreign body, an angiogram should be performed to determine if any vascular structures are involved. Moriarty and others (1997) have reported carotid artery thrombosis and stroke in a 2-year-old following blunt pharyngeal trauma from a fall with a toothbrush.
|
FIGURE 30-10 The left tonsillar bed of a 6-year-old girl was impaled after she fell with a toothbrush in her mouth. She was intubated orally with direct laryngoscopy. |
Dog bites are another common cause of facial injury in children. In a study by Mcheik and others in 2000 , the majority of children (68%) were less than 5 years of age. The goals of immediate surgical repair are to diminish scarring and decrease the rate of wound infection.
Last, extrusion of eye contents through a full-thickness penetrating ocular laceration may result in permanent loss of vision ( Fig. 30-11 ). Intraoperative anesthetic management of open globe injuries is discussed further in Chapter 22 , Anesthesia for Ophthalmic Surgery.
|
FIGURE 30-11 Open-eye injury in children is often caused by a projectile object. |
As with other trauma, facial injuries in children should be evaluated in the field or the emergency department during the primary survey. If there is any evidence of airway obstruction or respiratory insufficiency, the airway should be secured immediately with direct laryngoscopy, with LMA, or surgically. As mentioned previously, special attention to C-spine stability during direct laryngoscopy should be accomplished with inline stabilization of the neck. Once the airway is secured, a secondary survey can be performed to ascertain the extent of the facial injury and the need for surgical intervention.
▪ CHEST INJURIES
Chest injuries may be immediately life threatening due to impairment of breathing or circulation or as a result of exsanguinating hemorrhage. Life-threatening injuries that impair breathing include open or tension pneumothorax, flail chest, and injuries to the trachea or bronchi. Fortunately, most pediatric chest injuries (78%) can be managed safely with observation or tube thoracostomy ( Rielly et al., 1993 ).
Tension pneumothorax is an urgent yet manageable complication of chest injury that produces diminished breath sounds, tracheal deviation, hypotension, and increasing airway pressure to ventilate (i.e., decreased lung compliance). Tension pneumothorax occurs due to accumulation of air in the pleural space under pressure. Air from the injured lung is trapped in the pleural space by an air leak, which acts as a one-way valve such that each subsequent breath introduces air under progressively increasing pressure. This impairs breathing and venous return to the heart. It should be treated immediately with needle catheter decompression by inserting a large-bore intravenous catheter in the second intercostal space, followed by chest tube placement. Simple pneumothorax also causes lung collapse and impaired breathing but to a lesser degree than tension pneumothorax.
Open pneumothorax occurs when injury has produced a chest wall defect. This equalizes the pressure between the pleural space and the environment, causing collapse of the ipsilateral lung and to-and-fro movements of air with breathing through the chest wall defect rather than the airway. It is managed by covering the defect with an occlusive dressing taped on three sides. This allows the patient to breathe and prevents the accumulation of a tension pneumothorax.
The pediatric chest wall is more compliant than that of the adult. The chest wall has a significant cartilaginous component and the ribs are not completely ossified. Consequently, rib fractures and flail chest are less common in children than in adults. However, significant intrathoracic injury, such as pulmonary contusion, may occur in the absence of a rib fracture. Flail chest occurs when four or more ribs are each fractured in two places by blunt trauma. The floating fracture segments produce paradoxical movement of the chest wall and reduce ventilation of the lung. An underlying pulmonary contusion impairs gas exchange or ventilation.
Injury to the airway may result in severe impairment of breathing, airway obstruction or hemorrhage, or tension pneumothorax. This may be immediately or rapidly lethal. Establishing adequate ventilation may require placement of a double-lumen endotracheal tube or selective intubation of the main bronchus.
The mediastinum is highly mobile in children. Aortic tears are rare in children ( Eddy et al., 1990 ). When they occur, free rupture results in rapid demise of the patient. With contained rupture, the patients are frequently stable. Contained aortic injuries are managed operatively after life-threatening abdominal and head injuries are initially managed. A widened mediastinum, fractures of the first rib, or presence of an apical pleural “cap” on the left side each raises the possibility of an aortic disruption. An angiogram is essential for further evaluation ( Akins et al., 1981 ) ( Fig. 30-12 ). Significant cardiac injuries are uncommon in children ( Langer et al., 1989 ). Injuries to the heart, great vessels, or lung hilus may result in massive hemorrhage and impaired circulation. Penetrating chest injuries that usually occur as a result of violent acts are fortunately rare in children. In most cases, pneumothorax and hemothorax respond rapidly to the placement of chest tubes. Thoracotomy is required only in the infrequent cases of massive air leak, persistent bleeding with shock, or transfusion requirements exceeding 10 mL/kg per hour.
|
FIGURE 30-12 (A) This child presented with a widened mediastinum following blunt chest trauma. (B) An immediate arteriogram revealed a disrupted aortic arch. |
▪ ABDOMINAL INJURIES
Abdominal injuries are the cause of death in approximately 10% of trauma fatalities ( Cooper et al., 1994 ). Blunt trauma as a result of motor vehicle accidents (as passengers or pedestrians) and falls are the most common mechanisms of injury in children. The vast majority of children with solid visceral injuries and bleeding do not require a laparotomy ( Haller et al., 1994 ; Mehall et al., 2001 ; Mooney, 2002). The bleeding usually stops without surgical intervention. Nonoperative management of blunt trauma requires careful physical examination and imaging (usually CT scanning) for detection of injuries followed by observation and serial examination.
Trauma laparotomy is infrequently performed in pediatric trauma centers, occurring in 0.3% of trauma admissions ( Green and Rothrock, 2002 ). Laparotomies are performed when signs of bowel perforation (pneumoperitoneum, peritonitis) or hemodynamic instability occur due to suspected intra-abdominal injury. Gunshot wounds to the abdomen and lower chest, evisceration, and symptomatic stab wounds are also indications for laparotomy ( Furnival, 2001 ; Stafford et al., 2002 ). Patients with asymptomatic anterior stab wounds are evaluated by local wound exploration and serial examinations. Asymptomatic flank and back stab wounds are evaluated by local exploration, serial examination, or contrast CT ( American College of Surgeons Committee on Trauma, 1997 ). The introduction of laparoscopy may reduce the number of laparotomies or replace DPL in cases when physical examination is unreliable and there is a concern for possible intra-abdominal injuries (e.g., head-injured multitrauma patients, seat belt injuries, and abdominal tenderness). Indications for operative management of specific severe injuries (e.g., pancreatic head or ductal injuries, bile leak) and complications are beyond the scope of this chapter.
Most renal injuries and lacerations do not require immediate surgery ( Cass, 1983 ; Bergren et al., 1987 ). Injury to the blood supply of the kidney that results in devascularization requires an operation. Devascularizing injuries can be diagnosed by the kidney failing to opacify with contrast material ( Karp et al., 1986 ; Kisa and Schenk, 1986 ). Blood at the urethral meatus suggests trauma to the lower urinary tract ( McAninch and Carroll, 1988 ). Retrograde urethrography and voiding cystourethrography are required studies. Transsection of the bladder neck can occur with major pelvic trauma and is suggested by the inability to feel the prostate on rectal examination.
▪ TRAUMATIC BRAIN INJURY
TBI is the leading cause of mortality in the pediatric trauma patient ( Tepas et al., 1990 ), accounting for over 70% of the deaths. Although motor vehicle accidents are the most common mechanism of head injury, 30% to 50% of TBI cases in children under 4 years of age are attributed to falls or abuse ( Dashti et al., 1999 ). Multisystem injury due to trauma is almost always associated with head injury in children. The disproportionately large head and relatively weak neck musculature, with a high center of gravity in children less than 3 years, puts them at risk for coup-countercoup brain injuries even at low velocities ( Dykes, 1999 ). Other factors contributing to the increased risk of TBI in children include thinner cranial bones and less myelinated nerve tissue, making them more vulnerable to damage.
Diffuse brain injury, the most common type of TBI in children, can range from a mild concussion to diffuse axonal injury resulting in permanent disability ( Bruce, 1981 ). Focal cerebral contusions may be located in the area of impact (coup) or on the opposite side of the brain (countercoup), or both. Intracranial hemorrhage can present in the epidural, subdural, subarachnoid, or intracerebral spaces. Epidural hematomas occur as a result of a tear in the middle meningeal artery, but subdural hematomas usually result from a tear in the bridging veins. In case of an epidural hematoma, rapid decompression is usually required due to the arterial nature of the bleeding, to avoid death or permanent disability. In addition, children may sustain concomitant skull fractures, which if open may require early surgical intervention.
The three phases of TBI are (1) the primary injury, (2) the secondary injury due to cerebral response to trauma, and (3) the secondary injury due to the systemic response to trauma ( Vavilala and Lam, 2002). The goal of the clinician caring for a child with TBI is to minimize neurologic effects of secondary injury, because this contributes largely to eventual morbidity and mortality. TBI should be considered in all children after trauma regardless of the absence of neurologic signs and symptoms. Initial assessment of the pediatric patient should include the GCS ( Table 30-4 ), the most widely used and best known of all trauma scores ( Teasdale and Jennett, 1974) . This scale has been validated in many studies as a reliable measure of neurologic outcome and is an excellent tool for following the neurologic status of a patient with TBI. The GCS has been modified for pediatric patients ( Marcin and Pollack, 2002 ) but can also be used for the cognitively impaired child. A GCS score of 13 or greater is associated with mild brain injury; 9 to 12, moderate brain injury; and less than 8, severe. In all children with head injuries, a pediatric GCS should be assigned on arrival and at each reexamination. Significant or progressive intracranial injury, as suggested by localizing neurologic signs, a GCS less than 13, or a decrease in the GCS of 2 points from the initial level, is an indication for a CT scan of the head ( Dykes, 1999 ). Seizures are not uncommon in children after even minor TBI ( Bruce et al., 1979 ). Loss of consciousness and/or seizure activity may increase the risk of vomiting and subsequent aspiration.
TABLE 30-4 -- Glasgow Coma Scale (GCS) and Pediatric Glasgow Coma Scale
|
Best Response |
Adult GCS |
Pediatric GCS |
Score |
|
Eye |
No eye opening |
No eye opening |
1 |
|
Eyeopening to pain |
Eye opening to pain |
2 |
|
|
Eye opening to verbal command |
Eye opening to speech |
3 |
|
|
Eyes open spontaneously |
Eyes open spontaneously |
4 |
|
|
Verbal |
No verbal response |
No vocal response |
1 |
|
Incomprehensible sounds |
Inconsolable, agitated |
2 |
|
|
Inappropriate words |
Inconsistently consolable, moaning |
3 |
|
|
Confused conversation |
Cries, but is consolable, inappropriate interactions |
4 |
|
|
Oriented |
Smiles, oriented to sounds, follows objects, interacts |
5 |
|
|
Motor |
No motor response |
No motor response |
1 |
|
Extension to pain |
Extension to pain |
2 |
|
|
Flexion to pain |
Flexion to pain |
3 |
|
|
Withdrawal from pain |
Withdrawal from pain |
4 |
|
|
Localizing pain |
Localizing pain |
5 |
|
|
Obeys commands |
Obeys commands |
6 |
From Marcin JP, Pollack MM: Triage scoring systems, severity of illness measures, and mortality prediction models in pediatric trauma. Crit Care Med 30:S457–S467, 2002.
|
GCS ≥13, mild brain injury; GCS 9 to 12, moderate brain injury; GCS <8, severe brain injury. |
There should be a low threshold for intubation in the child with TBI, for airway protection and hyperventilation. Waxing and waning mental status, or a GCS score of less than 8, is an indication for intubation and hyperventilation (to prevent increased arterial carbon dioxide and the resultant cerebral vasodilatation and brain swelling). It must be remembered that the presence or suspicion of a basilar skull fracture is a contraindication for a nasal intubation. Although little can be done to minimize the cerebral damage due to the primary injury, every effort should be made to minimize subsequent brain injury due to hypoxic or ischemic insult. Systemic abnormalities such as shock, hypotension, hypoxemia, and hypercarbia as a result of coexisting injuries may lead to further brain injury and should be promptly managed as discussed previously.
The reaction of the brain to the initial trauma develops over a 3- to 5-day period with potential for loss of autoregulation, cellular edema, and breakdown of the blood-brain barrier ( Vavilala and Lam, 2002). Cerebral blood flow (CBF), ICP, cerebral metabolic rate (CMRO2), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and acid-base status all may be affected by diffuse cerebral swelling, which may occur in TBI. Also, reperfusion following ischemic brain injury may be accompanied by activation of the inflammatory cascade ( Jean et al., 1998 ). The resultant influx of calcium, free radicals, cytokines, and other harmful inflammatory mediators has been implicated in the exacerbation of existing neuronal damage. Animal studies have demonstrated some benefits in terms of neurologic improvement by administration of anti-inflammatory antibodies, but human studies have not adequately addressed their use. Indeed, corticosteroids have a limited role in the routine management of the child with head trauma because they do not improve neurologic outcome and may predispose the child to infection ( Bracco and Bissonnette, 2002 ).
Children with cerebral edema or intracranial hypertension may require an ICP monitor or ventriculostomy to be placed. Figure 30-13 depicts an algorithm for maintaining normal ICP/CPP in the pediatric patient. Figure 30-14 demonstrates changes in MAP, ICP, and CPP with age. By manipulating MAP and CBF with vasopressors and hyperventilation, draining cerebrospinal fluid, and decreasing CMRO2with sedatives or barbiturates, the goals of maintaining a normal ICP/CPP may be met. Refractory intracranial hypertension may require barbiturate coma, aggressive hyperventilation with CBF and/or jugular venous monitoring, or even decompressive craniectomy. Therapeutic hypothermia (to a temperature of 32° to 33°C for 24 hours) has been shown to improve long-term neurologic outcomes in a controlled randomized study involving 82 adults with TBI ( Marion et al., 1997 ). However, hypothermia should be used only in selected patients with TBI because it did not improve outcomes in patients in whom ICP could be controlled by conventional measures ( Shiozaki et al., 1999 ).
|
FIGURE 30-13 The University of Michigan C. S. Mott Children's Hospital algorithm for the treatment of intracranial hypertension in children. (Courtesy of C. S. Mott Children's Hospital, Ann Arbor, MI.) |
|
FIGURE 30-14 Age-related increases in mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and intracranial pressure (ICP). |
The mortality rate for children with severe head injuries (GCS score <8) is as high as 32% ( Ward, 1995 ). Despite this high mortality rate, the functional outcome in children is thought to be better than that in adults. It is therefore imperative that the clinician manage children with TBI by rapidly alleviating the effects of the primary insult and aggressively treating the secondary injuries. TBI is discussed further in Chapter 18 , Anesthesia for Neurosurgery.
▪ SPINAL INJURIES
Although vertebral fractures in children are less common than in adults, it may be prudent to assume that any pediatric patient with a major traumatic injury has a spinal injury until proven otherwise. Cervical spine fractures occur in 7% to 10% of children with TBI, with 20% of these patients presenting with a second noncontiguous spinal injury. There are several anatomic differences between the adult and pediatric C-spine that account for the differences in the type of injuries incurred by each group. The fulcrum of cervical mobility in an infant or a young child is at the level of C2-3, compared with C5-6 or C6-7 in an adult. For this reason, 60% to 70% of pediatric fractures occur in the C1 or C2 vertebrae compared with only 16% in the adult population ( Hasue et al., 1974 ). C-spine fractures are less common in children because of ligamental laxity, but this does not prevent spinal cord damage in this population. By the time the child has reached 8 years of age, the C-spine has fully matured (Eichelberger, 1993 ).
Fracture of the ondontoid process (dens) of the C2 vertebra is one of the most common vertebral injuries in children (Figs. 30-15 and 30-16 [15] [16]). This is due to the inherent weakness of the growth plate at the base of the dens. These are usually flexion injuries that rarely cause initial neurologic impairment. Spinal cord damage is associated with hyperextension of the neck and posterior displacement of the dens into the cord. It is imperative, therefore, that any spinal injury is not exacerbated by manipulation of the neck during interventions such as endotracheal intubation. The presence of neck or back pain, altered mental status, or abnormal peripheral neurologic findings (e.g., priapism, paresthesia, and/or dysesthesia) should necessitate C-spine immobilization and a radiographic examination of the spine. A pediatric C-spine evaluation protocol is presented in Figure 30-17 .
|
FIGURE 30-15 Magnetic resonance image of a 22-month-old boy who fell off of a grocery cart onto his head. Arrow points to a nondisplaced fracture of the ondontoid process in C2. |
|
FIGURE 30-16 Posterior view of C2 ondontoid (dens) fracture. (From Netter F, editor: The Ciba collection of medical illustrations, vol 1; nervous system. Summit, NJ, 1953, p 83.) |
|
FIGURE 30-17 The University of Michigan C. S. Mott Children's Hospital algorithm for cervical spine evaluation in a pediatric trauma patient. (Courtesy of C. S. Mott Children's Hospital, Ann Arbor, MI.) |
Radiographic evaluation of the C-spine should not take precedence over the ABCs, but studies should be performed in a timely fashion. In the absence of a fracture, the diagnosis of spinal cord injury in children is confounded by ligamental laxity, larger acceptable predental spaces, and C2-3 override ( Swischuk, 1986 ) ( Table 30-5 ). If intubation is required, the neck should be maintained in a neutral position with a cervical collar. Older children may tolerate awake, fiberoptic intubation with or without sedation. The very young or uncooperative child or any patient with bloody secretions in the airway may not be suitable for this technique and requires a rapid sequence induction with inline stabilization of the neck.
TABLE 30-5 -- Upper normal limits of cervical spine measurements in adults and children
|
|
Adults |
Children |
|
Predental space |
2.5 mm |
4 to 5 mm |
|
C2-3 override (flexion) |
3 mm |
4 to 5 mm |
|
Prevertebral space (extension) |
7 mm |
½ to 2/3 AP distance vertebralss body |
From Eichelberger MR: Pediatric trauma prevention, acute care, rehabilitation. St. Louis, 1993, Mosby–Year Book, p 45.
▪ LAWNMOWER-RELATED INJURIES
Lawnmowers cause more than 9400 injuries in children less than 18 years of age annually in the United States, with almost a fourth of these injuries occurring in children less than 5 years of age ( US Consumer Product Safety Commission, 1990-1999 ) ( Fig. 30-18 ). The age distribution is bimodal, with peaks at 2 and 15 years, probably representing injuries to bystanders versus injuries to operators. More than 7% of children who incur mower-related injuries require hospitalization, about twice the rate for consumer product-related injuries. Riding lawnmowers, commonly used for lawn and field maintenance in this country, are more powerful and complex to operate than are walk-behind mowers. With an injury rate of more than three times that of walk-behind mowers, they carry a higher risk of injury and possible death than walk-behind mowers ( Adler, 1994 ). In 1993, a U.S. Consumer Product Safety Commission report identified four mechanisms of injury due to riding lawnmowers: loss of mower stability, blade contact, layout and function of the mower controls, and running over or backing over young children ( Adler, 1993 ). Backover injuries occurred approximately twice as often as did runover injuries, with about 85% of these injuries occurring in children between 15 months and 10 years of age. Typically, this occurs when the child is playing in the area, is following the mower, or falls off the back of the mower ( Deppa, 1994 ).
|
FIGURE 30-18 Photograph of a 3-year-old child who was backed over by a riding lawnmower and sustained massive facial trauma and amputation of the left foot. |
The types of injuries incurred by children range from lacerations (41%) to amputations and avulsions (7%) ( US Consumer Product Safety Commission, 1990-1999 ). Aside from initial stabilization and treatment, children with these injuries may require repeated anesthetics for wound debridement, reductions of bony fractures, skin grafts, or reconstructive surgery. A child presenting with a lower extremity injury may benefit from combined epidural and general anesthesia, with continued epidural analgesia in the postoperative period. The following are some of the recommendations of the American Academy of Pediatrics Committee on Injury and Poison Prevention ( Smith and Prevention, 2001) .
|
|
1. |
Manufacturers of riding lawnmowers should sell only tractors that will not mow in reverse without a manual override. |
|
|
2. |
Children younger than 6 years of age should be kept indoors when lawnmowers are being operated. |
|
|
3. |
Children must not be allowed to ride on mowers as passengers. |
|
|
4. |
Children should not operate lawnmowers until they have displayed the necessary levels of judgment, strength, skill, and maturity. Most children will not be ready to operate a walk-behind mower until 12 years of age, and a riding mower until at least 16 years. |
▪ SKELETAL INJURIES
Musculoskeletal injuries are rarely life threatening except when they are associated with ongoing severe hemorrhage, yet they are a leading cause of morbidity and long-term disability, and if not managed appropriately and in a timely manner, long-term sequelae including limb deformities, permanent neurologic and joint dysfunction, and loss of limb viability may result. Additional considerations in children include premature growth arrest and potential for growth plate injuries. In the multiply injured child, it is important to identify the priorities of treatment. Control of bleeding as a result of skeletal injuries should occur as part of the primary survey. Once life-threatening injuries such as head and chest injuries are addressed and initially stabilized, the extent of skeletal injuries should be carefully assessed based on symptoms, physical examination, and radiography. Appropriate initial measures include functional bracing or splinting to alleviate pain and immobilization of bone fragments to prevent further injury of adjacent neurovascular structures, allow safe transport of the patient, and minimize impairment of limb function. In patients with adequate alignment of fracture segments, this may be the only necessary treatment. Other interventions that may be needed in case of displaced fractures include external traction, external fixation, and internal fixation.
Urgent or emergent surgical interventions are usually indicated in the case of complex or displaced fractures associated with vascular damage and potential for limb ischemia or neurologic dysfunction, open fractures, joint dislocations that cannot be reduced, and compartment syndromes ( Musgrave and Mendelson, 2002 ). Vascular injuries in conjunction with limb fractures are, fortunately, rare in children. Although the majority of vascular injuries are associated with supracondylar distal humerus fractures, they may also occur in conjunction with fractures of the distal femur, proximal tibia, displaced pelvic fractures, and knee dislocations. Children with suspected vascular injuries may require an angiogram to delineate the extent of the injury and to determine the need for revascularization. In the case of open fractures, wound irrigation and debridement with extensive removal of contaminated and necrotic tissue are required. Children with open fractures frequently require repeated debridement under general anesthesia every 48 to 72 hours until all of the devitalized tissue has been removed. Pain out of proportion to the extent of the injury should raise concern about compartment syndrome. In these cases, emergent fasciotomies of all involved compartments is indicated because significant muscle necrosis can occur if intracompartment pressures exceed 30 mm Hg for longer than 8 hours ( Musgrave and Mendelson, 2002 ).
Fractures of the femur in children most commonly involve the femoral shaft or the distal femoral physis. Femoral shaft fractures can result in significant blood loss from the fracture segments, and such blood loss may not be readily recognized because the blood accumulates in the large thigh compartments. Serial hematocrits should be obtained in children with femur fractures, and they should be adequately volume resuscitated before the induction of anesthesia to avoid cardiovascular collapse on induction. A high index of suspicion for compartment syndrome should be maintained, particularly in the patient with concomitant head trauma who may be difficult to evaluate. Children with distal femur fractures are at risk of arterial injury and compartment syndrome; attention should be focused on the neurovascular status of the limb ( Musgrave and Mendelson, 2002 ).
The issue of early versus delayed stabilization of femur fractures in children with closed head injuries remains contentious. Interpretation of the existing literature is confounded by variability in study design, small sample size of patients studied, differences in severity of head injury in the early versus late treatment groups, and variable definitions of early versus late treatment. Previous studies in adults have found that early fixation significantly reduced the incidence of severe pulmonary complications, including respiratory distress syndrome, pneumonia, and pulmonary emboli ( Bone et al., 1989 ;Behrman et al., 1990 ). Pediatric studies found that early stabilization did not lessen the risk of pulmonary complications in the multiply injured child. A retrospective study by Hedequist and others (1999)identified 25 children with femur fractures and central nervous system injury (GCS score, 8). Seven of these children underwent early stabilization, of whom 4 (57%) experienced a respiratory complication compared with 8 complications in 18 (44%) who underwent delayed fixation. In another retrospective study in children, Mendelson and others (2001) reported twice the number of respiratory complications in the late treatment group (4 of 13 versus 2 of 12, P = NS). This difference may be clinically significant, but the groups were dissimilar in that children in the late treatment group had a higher incidence of increased intracranial pressure. Other purported benefits of early fixation include early patient mobilization, shorter hospital and intensive care unit stays, improved predictability of fracture outcome, and decreased costs.
Proponents of late stabilization argue that minor hemodynamic changes, including shifts in blood pressure and volume status, may potentiate secondary brain injury and lead to adverse neurologic outcomes. Previous investigators have reported a greater frequency of intraoperative hypotension and hypoxemia and lower mean GCS scores in patients undergoing early fracture stabilization ( Jaicks et al., 1997 ;Townsend et al., 1998 ). Yet, other studies have found no relationship between timing of fracture fixation and head trauma outcome ( McKee et al., 1997 ; Kalb et al., 1998 ; Mendelson et al., 2001 ). The Committee on Trauma of the American College of Surgeons has recommended that femoral fractures be treated early provided hemodynamic stability has been achieved ( Burgess and Cates, 1993 ). The appropriate timing of femur fracture fixation in a head-injured child remains open to further investigation. Until more definitive data become available, it may be prudent to delay operative fixation of femur fractures until stabilization of hemodynamic and neurologic status are achieved. Also, adequate volume resuscitation and careful monitoring of end-organ perfusion and pressure, including blood pressure and ICP monitoring, should be strongly considered to guide intraoperative interventions that reduce the risk of secondary brain injury.
Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com
Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.
Copyright © 2005 Mosby, An Imprint of Elsevier
▪ PERIOPERATIVE MANAGEMENT
Children with multiple injuries frequently present with an unusual combination of anesthetic problems that present a challenge to the anesthesiologist. It must be emphasized that the likelihood of a successful outcome is greatly enhanced by the initial stabilization efforts that must include early initiation of critical care management in the emergency department based on appropriate and rapid physical examination and diagnostic studies rather than an urgent rush to the operating room for emergency surgical interventions ( Meyer, 1999 ). Respiratory stabilization and suitable hemodynamic support including volume resuscitation prevent further decompensation and the development of secondary injuries. This in turn requires a well-coordinated effort by all members of the health care team, including the anesthesiologist, the emergency physician, surgeons of the relevant specialties, respiratory therapists, and critical care physicians and nurses. Only in rare instances is there too little time for the initial stabilization such that a child must undergo surgery emergently to ensure a favorable outcome. In such instances, there must be clear communication between the anesthesiologist and surgeon regarding the time available for resuscitation, securing vascular access, and invasive monitoring capabilities.
Ideally, the role of anesthesiologists in the care of the child who has sustained significant trauma should begin with securing the airway in the emergency department. However, if this cannot be accomplished, it is imperative that they become familiar with the immediate and ongoing resuscitative efforts, as well as the extent and nature of the injuries and the pertinent details regarding the patient's past medical history. The following addresses the anesthetic management of the child who presents for emergent surgery following multiple trauma. The major concerns include (1) NPO status, (2) airway management, (3) anesthetic agents, (4) patient monitoring, and (5) fluid and blood resuscitation.
▪ NPO STATUS
It is common practice to consider all trauma patients at risk for aspiration regardless of the time of last oral intake. The rationale for this approach is that major injury, the presence of pain and anxiety, and/or the administration of opioid analgesics delay gastric emptying. Additionally, bag and mask ventilation at the scene of the accident or in the ED leading to gastric distention, and the use of oral contrast solutions for diagnostic imaging studies may further increase the risk for aspiration. Indeed, previous investigators have demonstrated that patients who present for emergency surgery are at five times the risk for aspiration compared with those who undergo elective surgery ( Olsson et al., 1986 ). Other investigators reported a 17% incidence of vomiting and 3% incidence of aspiration in 60 children less than 19 years of age who required emergency endotracheal intubation after they sustained a severe traumatic injury ( Nakayama et al., 1992 ). Interestingly, residual gastric volume has been previously found to have a greater correlation with the interval from oral intake to injury than with actual fasting interval ( Bricker et al., 1989 ).
These data raise two questions regarding the management of anesthetic induction for the trauma patient: Can we predict the safe interval between oral intake, injury, and induction of anesthesia? Does imposing a fasting duration once the trauma has already occurred offer any benefit in terms of reduction in aspiration risk? Goodwin and Robinson (2000) surveyed 167 practicing anesthesiologists in the United Kingdom regarding their practice in three different scenarios following a forearm fracture in a child. Approximately one third of the respondents did not believe there was any benefit in delaying the procedure and would perform a rapid sequence induction and endotracheal intubation regardless of the fasting duration, whereas almost two thirds of the respondents would delay the procedure if it were not emergent and then use an LMA or facemask as they would for elective cases. Such variability in clinical practice related to the management of the trauma patient is likely due to the difficulty in predicting a safe interval between oral intake, injury, and induction of anesthesia with regard to aspiration risk. All trauma patients should have full stomach precautions and be considered at risk for aspiration.
▪ ANESTHETIC AGENTS
Induction of Anesthesia
Anesthetic induction techniques should be individualized depending on the nature of the injuries, whether the airway has been secured before arrival in the operating suite, anticipated airway difficulty, hemodynamic status of the patient, and the presence of ongoing hemorrhage. The child with head trauma merits special consideration due to the risk of increased ICP during induction of anesthesia. Selection of an induction technique in these patients must be made with the goal of avoiding secondary brain injury. Intravenous induction agents such as thiopental, propofol, or etomidate may be preferred due to their beneficial effects on ICP and CMRO2. On the other hand, a child with an anticipated difficult airway may be more easily managed with an inhaled route of induction so that spontaneous breathing is ensured. Induction of anesthesia in a patient with dehydration or hypovolemia may lead to cardiovascular collapse. It is therefore imperative to have adequate intravenous access and to rehydrate these patients before the induction of anesthesia. A brief description of commonly used induction agents and pitfalls with the use of each in a child with trauma follows (see Chapter 6 , Pharmacology of Pediatric Anesthesia, and Chapter 11 , Intraoperative and Postoperative Management).
Thiopental.
The barbiturates have a long history of use as neuroprotectants. Thiopental has been extensively used as an induction agent in head-injured patients because it is a cerebral vasoconstrictor and decreases CBF, CMRO2, and ICP in a dose-dependent manner. Another beneficial central nervous system effect is reduction in epileptiform activity. Furthermore, thiopental reliably attenuates the increase in ICP caused by noxious interventions such as direct laryngoscopy and endotracheal tube placement. Thiopental should be used with caution in a child with multiple trauma because it is a direct myocardial depressant and may produce a decrease in cardiac output and systemic blood pressure with a resultant decrease in CPP. These effects are more pronounced in patients who have been inadequately volume resuscitated, and the use of alternative induction agents such as etomidate should be strongly considered in patients with a questionable volume status or with uncontrolled, ongoing hemorrhage.
Propofol.
Induction of anesthesia with propofol even in healthy children is frequently associated with a significant (10% to 20%) decrease in MAP due to its direct relaxant effects on vascular smooth muscle, causing a reduction in systemic vascular resistance and preload. It should, therefore, be used with caution, if at all, in patients with depleted intravascular volume. Its beneficial effects of cerebral vasoconstriction, reduced CBF, and CMRO2 in patients with head trauma are offset to an extent by a reduction in CPP due to a decrease in systemic blood pressure. It has been further hypothesized that the decrease in CPP may lead to reflex cerebral vasodilation to maintain CBF, thereby also negating its beneficial effects in reducing ICP ( Spitzfaden et al., 1999 ).
The adult literature evaluating the use of propofol in neurosurgical patients has yielded conflicting results. Previous studies have demonstrated that while propofol effectively lowered ICP in patients with elevated ICP following TBI and during cerebral aneurysm surgery, there was a reduction in CPP because of the greater decrease in MAP than in ICP caused by propofol ( Herregods et al., 1988 ; Ravussin et al., 1988 ; Pinaud et al., 1990 ). Other investigators reported no reduction in ICP with propofol sedation in adults with head trauma ( Stewart et al., 1994 ). Finally, in adult closed head injury patients administered propofol along with other measures to lower ICP (e.g., mannitol and hyperventilation), these combined measures provided significant reductions in ICP without affecting MAP. Consequently, CPP improved ( Farling et al., 1989 ).
Data are limited with regard to the neurologic effects of propofol in children. Spitzfaden and others (1999) reported that propofol sedation produced significant reductions in ICP in two children with elevated ICP that had been previously refractory to other measures such as hyperventilation, mannitol, and sedation with midazolam and morphine. However, the effects of propofol on MAP were not reported in one child, and the other child required dopamine to maintain MAP so that CPP was not compromised. Taken together, the results of these studies suggest that further data are required to evaluate the use of propofol in the patient with reduced intracranial compliance.
Etomidate.
Etomidate provides both hemodynamic stability and cerebral protection, making it the ideal anesthetic induction agent for emergency surgery in a child with multiple trauma. Although it does cause a direct myocardial depressant effect, it does so to a significantly lesser extent than equipotent doses of other induction agents, including thiopental, propofol, and ketamine ( Stowe et al., 1992 ). Etomidate, however, maintains sympathetic outflow and produces no significant changes in blood pressure making it the agent of choice in the hemodynamically unstable patient. Similar to thiopental and propofol, it is a cerebral vasoconstrictor and causes a reduction in ICP, CBF, and CMRO2. However, because MAP is maintained with etomidate, CPP is also maintained. Perhaps the only concern with its use has been adrenal suppression; however, this is believed to have questionable clinical significance with brief use ( Crozier et al., 1987 ). A recent retrospective review reported successful fracture reduction in 52 of 53 patients who received etomidate alone or in combination with midazolam and/or opioids ( Dickinson et al., 2001 ). This study found a low incidence of minor side effects, including nausea and vomiting, mild hypotension, and prolonged sedation in one patient each.
Ketamine.
Ketamine is a dissociative anesthetic that is frequently selected for induction in hypovolemic children because its sympathomimetic actions result in an increase in blood pressure and heart rate. However, like the other induction agents described earlier, ketamine has direct myocardial depressant effects and direct vasodilatory effects. In fact, significant hypotension has been reported following ketamine administration in critically ill patients, likely due to its direct myocardial-depressant effects, which occur in the presence of depleted catecholamine stores ( Waxman et al., 1980 ).
Ketamine, however, is a potent cerebral vasodilator causing a marked increase in CBF. While CMRO2 usually remains unchanged following ketamine administration, ICP may increase, especially in patients with intracranial pathology. However, data regarding the effects of ketamine on ICP remain inconclusive, with some studies demonstrating modest decreases in ICP following ketamine administration, particularly when administered concomitantly with other sedatives ( Mayberg et al., 1995 ; Albanese et al., 1997 ). A controlled, randomized, double-blind trial found no differences in mean daily values of ICP, CPP, and number of episodes of ICP elevations in patients with severe TBI sedated with ketamine and midazolam compared with those sedated with sufentanil and midazolam ( Bourgoin et al., 2003 ). Yet, its cerebral vasodilatory effects preclude the use of ketamine as an induction agent in patients with head trauma.
Maintenance of Anesthesia
Selection of agents for maintenance of anesthesia should be based on the nature and duration of the proposed procedure; the extent of injuries; the child's ventilatory, hemodynamic, and neurologic status; and whether postoperative mechanical ventilation is anticipated. In hemodynamically stable patients, a standard general anesthetic may be used, including volatile agents, opioids for postoperative pain relief, and muscle relaxants as needed to provide good operating conditions. A technique using an opioid, hypnotic, muscle relaxant and oxygen may be more suitable in a child with unacceptably low blood pressure who may not tolerate the negative inotropic effects of potent volatile anesthetics. In such cases, fentanyl or sufentanil would be the preferred opioid because these do not significantly alter hemodynamic parameters, especially blood pressure. In children with uncertain injuries, nitrous oxide is best avoided because it may diffuse into closed air spaces such as the pleural cavity. In such cases, the use of amnestic agents such as benzodiazepines is useful in reducing the likelihood of awareness.
In a child with severe head trauma, efforts must be directed at preventing secondary brain injury and protecting the injured brain from further ischemia by selecting anesthetic techniques that maintain cardiovascular stability while reducing ICP. All volatile anesthetics cause cerebral vasodilation that is dose (minimum alveolar concentration [MAC]) related ( Vavilal and Lam, 2002) . Isoflurane affects CBF and cerebral autoregulation to a lesser extent than does halothane. Sevoflurane offers greater advantages in that CBF velocities do not increase significantly with less than 1 MAC ( Monkhoff et al., 2001 ), and cerebral pressure autoregulation is maintained up to 1.5 MAC sevoflurane. For these reasons, sevoflurane may be the preferred volatile anesthetic for the child with TBI and it would be prudent to limit its use to 1 MAC.
Opioids (fentanyl, sufentanil, or remifentanil) are frequently administered as intermittent bolus doses or continuous infusions to supplement volatile anesthetics, for postoperative analgesia, and as additional measures to lower ICP. Increased ICP has been reported in an 11-year-old with closed head injury following fentanyl administration that responded to hyperventilation and barbiturates ( Tobias, 1994 ). In addition, studies in adults have reported a transient but very significant increase in ICP accompanied by a decrease in MAP and CPP following bolus doses of morphine, fentanyl, sufentanil, and alfentanil (Albanese et al., 1999 ; de Nadal et al., 2000 ). The exact mechanism of these changes remains unknown, but impaired cerebrovascular autoregulation and direct cerebral vasodilatory effects of opioids have been implicated. Such effects may have important implications in the management of the child with head trauma. Until additional data become available, the judicious use of opioid infusions with careful monitoring of hemodynamic parameters is recommended.
▪ PATIENT MONITORING
In addition to routine monitors, placement of invasive monitors, including arterial and central venous catheters, and a urinary catheter must be considered in the child with extensive injuries and those with head trauma. Placement of such catheters should be efficient, and in some cases when the surgery must be performed expeditiously, invasive monitors may need to be placed while the procedure is already under way. An arterial catheter is invaluable in cases of head, chest, and extensive abdominal trauma. Invasive catheters allow for continuous blood pressure management and frequent arterial blood gas, electrolyte, and serial hematocrit determination. Central venous pressure monitoring is useful in patients in whom large fluid shifts are expected and when rapid ongoing blood loss is anticipated. Central venous access also allows for mixed venous blood gas determination. Urine output is an important measure of fluid status. The need for additional monitors such as ICP and somatosensory evoked potential monitors must be individualized. In some cases of chest trauma, echocardiography may be useful in diagnosing injuries such as cardiac contusion causing ventricular wall motion abnormalities, aortic aneurysm, and cardiac tamponade.
Temperature monitoring and preventing hypothermia are an important aspect of trauma resuscitation but one that is frequently overlooked due to other priorities such as resuscitation. In the traumatized child, several factors contribute to ongoing heat loss and subsequent hypothermia. These factors include exposure to a cold environment at the scene of the accident, large open wounds, rapid infusion of cold intravenous fluids and blood products, and exposure of body cavities with consequent evaporative heat loss during operative procedures. Hypothermia has significant deleterious effects that may hinder resuscitative efforts. Such effects include myocardial dysfunction, cardiac irritability, and dysrhythmias. Other effects of hypothermia include acid-base disturbances, unpredictable dose-response curves of the anesthetic agents, a leftward shift of the oxyhemoglobin dissociation curve, and coagulopathies. Continuous temperature monitoring in all pediatric trauma patients is therefore essential. Every effort should be made to maintain temperature, including use of warm intravenous fluids, keeping the child covered once initial evaluation is completed, maintaining a warm environment, use of radiant warmers for infants, and the use of forced air warming devices. If possible, the head should be wrapped in plastic, and if the intestines are exposed, they should be placed in a plastic bag to help reduce heat loss by radiation and evaporation.
▪ FLUID AND BLOOD RESUSCITATION
Shock is defined as a metabolic demand that exceeds either oxygen supply or oxygen delivery ( Rasmussen and Grande, 1994 ). When a child who has sustained multiple injuries presents for surgical intervention, the fluid status must be quickly assessed before induction of anesthesia based on a physical examination and on fluid resuscitation administered before arrival in the operating suite. The anesthesiologist must be prepared to continue the fluid resuscitation in case of ongoing blood loss or third space fluid losses. The goals of fluid resuscitation should be to maintain normovolemia and osmolar and oncotic pressures in the intravascular space. Crystalloid solutions such as lactated Ringer's solution or normal saline are most commonly used in the initial stages of resuscitation. Hypertonic saline solutions (3%) have also been used in this setting based on the premise that they increase serum osmolality and thereby maintain intravascular volume for longer periods and with smaller volumes administered than isotonic solutions ( Rasmussen and Grande, 1994 ). However, the data that support these arguments are inconclusive and further research in this area is needed. The decision to administer glucose-containing solutions must be based on serial blood glucose values. The issue of glucose administration is of greatest importance in the presence of head trauma because elevated blood glucose levels have been found to correlate significantly with indicators of the severity of brain injury and poor neurologic outcomes in children with severe brain injuries ( Michaud et al., 1991 ) (see Chapter 18 , Anesthesia for Neurosurgery).
Colloid solutions such as 5% albumin and hydroxyethyl starch have also been used for fluid resuscitation. Hydroxyethyl starch may exacerbate existing coagulopathy by interfering with platelet function, decreasing fibrinogen activity, and interfering with factor VIII ( Niemi and Kuitunen, 1998 ; Deusch et al., 2003 ). It is therefore unsuitable for the pediatric trauma patient. The purported benefits of colloid solutions include their ability to increase colloid oncotic pressure, prolonged maintenance of intravascular volume, and smaller volumes required compared with crystalloid solutions ( Niemi and Kuitunen, 1998 ). For these reasons, colloids may also be beneficial in children with head trauma because the smaller volume of fluids administered may reduce the likelihood of cerebral edema. One of the major concerns with the use of colloids has been the cost. In most patients who require massive fluid resuscitation, the cost of using colloids to supplement crystalloids may be justified. The discussion of the crystalloid versus colloid controversy has been reviewed elsewhere ( Imm and Carlson, 1993 ; Rizoli, 2003 ).
Blood Administration
The primary purposes for transfusion of blood products in a pediatric trauma patient are to maintain oxygen delivery and to ensure hemostasis. Packed red blood cells (PRBCs) are required when oxygen-carrying capacity is inadequate to meet tissue demands and metabolic rate. Losses of up to 40% of blood volume can usually be replaced with isotonic crystalloid solutions or colloids without physiologic signs of inadequate oxygen delivery ( Solheim and Wesenberg, 2001 ). When estimated blood volume losses exceed 40%, the decision to transfuse blood should be based on an overall assessment of the patient that includes the hemodynamic status, extent of ongoing blood loss, and underlying comorbidity. Some children may require blood transfusion with blood volume losses less than 40% if the blood loss has been rapid or if they have a significant underlying medical condition such as congenital cyanotic heart disease or blood dyscrasias. Although there can be no fixed numerical transfusion trigger in all trauma patients, Table 30-6 presents formulas that may be used as general guidelines to calculate allowable blood losses ( Rasmussen and Grande, 1994 ). In most centers, blood banks supply blood components rather than whole blood. The primary advantage of component therapy is more efficient and cost-effective use of resources by eliminating the transfusion of unnecessary components and making components from a single blood donation available to several patients. It also permits improved preservation of individual components.
TABLE 30-6 -- Formulas to use as a general guideline to calculate allowable blood loss
|
Calculation 1[*] |
ABL = EBV ×· (HCT initial- HCT target) HCT initial |
Calculations for allowable blood volume from Rasmussen GE, Grandes CM: Blood, fluids, and electrolytes in the pediatric trauma patient. Int Anesthesiol Clin 32:79–101, 1994.
|
ABL, allowable blood loss; EBV, estimated blood volume; HCT, hematocrit; ERCM, estimated red cell mass; ARCL, allowable red cell loss. |
|
* |
The ABL, in milliliters, must be multiplied by 3 if replacement is by crystalloid and replaced, 1:1 if blood is to be used. |
The unstable patient in hemorrhagic shock may need blood before cross-matching procedures can be completed. The possibility of encountering a clinically significant, non-ABO antibody is rare in children. Type O Rh-negative non-cross-matched blood is preferred for emergency transfusions ( Schwab et al., 1986 ).
Packed Red Blood Cells
The indication to transfuse PRBCs is to increase oxygen-carrying capacity. PRBCs are supplied in units of approximately 250 mL with hematocrits ranging from 60% to 80%. The units are preserved either in CPD (citrate, phosphate, and dextrose) with a shelf-life of 21 days or in CPD-A (citrate, phosphate, dextrose, and adenine) with a shelf-life of 35 days. The citrate in the preservative chelates calcium; therefore intravenous calcium supplement (calcium gluconate or chloride) must be readily available when transfusing PRBCs, especially at a rapid rate. The usual starting dose of PRBCs is 10 to 20 mL/kg depending on rapidity of blood loss. Banked red blood cells have a number of features with significant clinical effects, as summarized in Table 30-7 .
TABLE 30-7 -- Differences in composition of major blood products
|
|
Normal Whole Blood (in vivo) |
Citrated Whole Blood (2 Weeks Old) CPD |
Citrated Packed Red Blood Cells[*] |
Frozen Packed Red Blood Cells |
FFP |
|
pH |
7.4 |
6.6–6.9 |
6.6–6.9 |
6.6–7.2 |
6.6–6.9 |
|
PCO2 |
35–45 |
180–210 |
180–210 |
0–10 |
180–210 |
|
Base deficit (mmol/L) |
0 |
9–15 |
9–15 |
? |
9–15 |
|
Potassium (mmol/L) |
3.5–5.0 |
18–26 |
18–26 (mmol/L) |
1–2 mmol/L |
4–8 |
|
Citrate |
None |
+ + + + |
+ + |
None |
+ + + + |
|
Factors V and VIII |
Normal |
20%–50% |
20%–50% |
None |
85%–100% |
|
Fibrinogen |
Normal |
Normal |
Normal |
None |
Normal |
|
Platelets |
240,000–400,000 |
None |
None |
None |
None |
|
2,3-DPG |
Normal |
3% of normal |
3% of normal |
Nearly normal |
— |
|
Hematocrit |
35–45 |
35–45 |
60–70 |
50–95 |
— |
|
Temperature |
37°C |
4°–6°C |
4°–6°C |
4°–6°C |
Cold |
(From Coté CJ, Ryan JF, Todre DD, et al.: A practice of anesthesia for infants and children, 2nd edition, New York, 1993, Grune & Stratton, p 186. Modified from Miller RD: Refresher Courses in Anesthesiology 1:101, 1973.)
|
CPD: Citrate-phosphate-dextrose; FFP: fresh frozen plasma |
|
* |
Citrated whole blood and citrated packed red blood cells have the same chemical composition, but citrated red blood cells have considerably less plasma volume. |
Fresh Frozen Plasma
Fresh frozen plasma (FFP) must be separated from whole blood within 6 to 8 hours of collection. It generally takes approximately 45 minutes to thaw because it is stored at -18°C, and it must be used within 24 hours once thawed. FFP provides factors II, V, VIII, IX, X, and XI and antithrombin III. Most clotting factors are stable in banked CPD blood, but levels of factors V and VIII fall, reaching 15% and 50% of normal levels, respectively, at 21 days after collection. Only 20% of factor V and 30% of factor VIII are required to support adequate coagulation, so clotting tests should guide the replacement of clotting factors with FFP. In general, FFP should be transfused when clotting studies become abnormal, including a prolonged prothrombin time (PT) or activated partial thromboplastin time (aPTT). Nonsurgical bleeding in children who receive more than 1 blood volume of PRBCs frequently require FFP due to factor V and VIII deficiency. The recommended initial dose of FFP is 10 to 15 mL/kg. Constituents of FFP are listed in Table 30-7 .
Platelets
Platelets are prepared through centrifugation and recentrifugation of fresh whole blood. Dilutional thrombocytopenia is the most likely cause of nonsurgical or microvascular bleeding following massive blood transfusion, and usually platelets are required before FFP for this condition. Transfusion of 0.1 unit/kg will raise the platelet count by approximately 20,000. Because platelet counts of 50,000 are adequate to achieve surgical hemostasis, doses in excess of 0.2 unit/kg are rarely required.
Cryoprecipitate
Cryoprecipitate that is produced by refreezing the insoluble portion of plasma is rich in factor VIII and fibrinogen. The insoluble portion from 1 unit of FFP yields 100 units of cryoprecipitate. The primary indications for cryoprecipitate in the trauma patient are bleeding abnormalities following massive transfusion, disseminated intravascular coagulation (DIC), and decreased fibrinogen levels. The recommended initial dose of cryoprecipitate is 0.1 unit/kg.
Massive Blood Replacement
Massive blood replacement is defined as the administration of 1 blood volume or more within a 24-hour period. It causes a number of physiologic derangements that can be detrimental in the child with multiple injuries, including coagulation defects, electrolyte and acid-base abnormalities, and hypothermia. Dilutional thrombocytopenia and clotting factor deficiencies have been primarily implicated in the etiology of nonsurgical bleeding following massive blood transfusion. However, mathematical models have demonstrated that a third of the patient's own blood remains after a single blood volume exchange, thereby retaining sufficient platelets and clotting factors to permit hemostasis ( Marsaglia and Thomas, 1971 ). Other factors such as incompatibility of transfused blood and DIC have also been implicated in the etiology of nonsurgical bleeding in the trauma patient.
Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com
Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.
Copyright © 2005 Mosby, An Imprint of Elsevier
▪ SUMMARY
Pediatric trauma accounts for 25% of all trauma cases in the United States. ATLS should be thought of as a continuum, beginning with the traumatic event; continuing through resuscitation and stabilization in the emergency department, diagnostic areas, and the operating room; and ending at discharge of a stable patient in the recovery room or intensive care unit. Careful evaluation with good teamwork and meticulous attention to detail can contribute to a positive outcome.
Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com
Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.
Copyright © 2005 Mosby, An Imprint of Elsevier
REFERENCES
Adler, 1993. Adler P: Ride-on mower hazard analysis (1987–1990), Washington, DC, Directorate for Epidemiology, US Consumer Product Safety Commission, 1993.
Adler, 1994. Adler P: Ride-on mower hazard analysis (1991–1993), Washington, DC, Directorate for Epidemiology, US Consumer Product Safety Commission, 1994.
Akins et al., 1981. Akins CW, Buckley MJ, Daggett W, et al: Acute traumatic disruption of the thoracic aorta: A ten-year experience. Am Coll Surg 1981; 31:305.
Albanese et al., 1997. Albanese J, Arnaud S, Rey M, et al: Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology 1997; 87:1328-1334.
Albanese et al., 1999. Albanese J, Viviand X, Potie F, et al: Sufentanil, fentanyl, and alfentanil in head trauma patients: A study on cerebral hemodynamics. Crit Care Med 1999; 27:262-263.
American College of Surgeons Committee on Trauma, 1997. American College of Surgeons Committee on Trauma : Advanced trauma life support for doctors, Chicago, American College of Surgeons, 1997.
Anderson, 1995. Anderson PJ: Fractures of the facial skeleton in children. Injury 1995; 26:47-50.
Anderson, 2001. Anderson RN: Deaths: Leading causes for 1999. Natl Vital Stat Rep 2001; 49:1-87.
Aun et al., 1993. Aun CS, Sung RY, O'Meara ME, et al: Cardiovascular effects of I.V. induction in children: Comparison between propofol and thiopentone. Br J Anaesth 1993; 70:647-653.
Behrman et al., 1990. Behrman SW, Fabian TC, Kudsk KA, et al: Improved outcome with femur fractures: Early vs. Delayed fixation. J Trauma 1990; 30:792-797.
Bergren et al., 1987. Bergren CT, Chan FN, Bodzin JH: Intravenous pyelogram results in association with renal pathology and therapy in trauma patients. J Trauma 1987; 27:515-518.
Bone et al., 1989. Bone LB, Johnston KD, Weigelt J, Scheinberg R: Early versus delayed stabilization of femoral fractures. A prospective randomized study. J Bone Joint Surg Br 1989; 71:336-340.
Bourgoin et al., 2003. Bourgoin A, Albanese J, Wereszczynski N, et al: Safety of sedation with ketamine in severe head injury patients: Comparison with sufentanil. Crit Care Med 2003; 31:711-717.
Bracco and Bissonnette, 2002. Bracco D, Bissonnette B: Neurosurgery and neurotraumatology: Anesthetic considerations and postoperative management, New York, McGraw-Hill, 2002.
Bricker et al., 1989. Bricker SR, McLuckie A, Nightingale DA: Gastric aspirates after trauma in children. Anaesthesia 1989; 44:721-724.
Bruce et al., 1979. Bruce DA, Raphaely RC, Goldberg AI, et al: Pathophysiology, treatment and outcome following severe head injury in children. Childs Brain 1979; 5:174-191.
Bruce, 1981. Bruce DA: Diffuse cerebral swelling following head injuries. J Neurosurg 1981; 54:170-178.
Bulas et al., 1989. Bulas DI, Taylor GA, Eichelberger MR: The value of CT in detecting bowel perforation in children after blunt abdominal trauma. AJR Am J Roentgenol 1989; 153:561-564.
Burgess and Cates, 1993. Burgess RC, Cates H: Deformities of the forearm in patients who have multiple cartilaginous exostosis. J Bone Joint Surg Am 1993; 75:13-18.
Cass, 1983. Cass AS: Blunt renal trauma in children. J Trauma 1983; 23:123-127.
Chu et al., 1996. Chu UB, Clevenger FW, Imami ER, et al: The impact of selective laboratory evaluation on utilization of laboratory resources and patient care in a level-I trauma center. Am J Surg 1996; 172:558-562.discussion 562–553
Coley et al., 2000. Coley BD, Mutabagani KH, Martin LC, et al: Focused abdominal sonography for trauma (FAST) in children with blunt abdominal trauma. J Trauma 2000; 48:902-906.
Cooper et al., 1994. Cooper A, Barlow B, DiScala C, String D: Mortality and truncal injury: The pediatric perspective. J Pediatr Surg 1994; 29:33-38.
Criswell et al., 1994. Criswell JC, Parr MJ, Nolan JP: Emergency airway management in patients with cervical spine injuries. Anaesthesia 1994; 49:900-903.
Crozier et al., 1987. Crozier TA, Beck D, Schlaeger M, et al: Endocrinological changes following etomidate, midazolam, or methohexital for minor surgery. Anesthesiology 1987; 66:628-635.
Dashti et al., 1999. Dashti SR, Decker DD, Razzaq A, Cohen AR: Current patterns of inflicted head injury in children. Pediatr Neurosurg 1999; 31:302-306.
de Nadal et al., 2000. de Nadal M, Munar F, Poca MA, et al: Cerebral hemodynamic effects of morphine and fentanyl in patients with severe head injury: Absence of correlation to cerebral autoregulation. Anesthesiology 2000; 92:11-19.
Deppa, 1994. Deppa RW: Options package for riding mowers, Washington, DC, Directorate for Engineering Sciences, US Consumer Product Safety Commission, 1994.
Deusch et al., 2003. Deusch E, Gamsjager T, Kress HG, Kozek-Langenecker SA: Binding of hydroxyethyl starch molecules to the platelet surface. Anesth Analg 2003; 97:680-683.
Dickinson et al., 2001. Dickinson R, Singer AJ, Carrion W: Etomidate for pediatric sedation prior to fracture reduction. Acad Emerg Med 2001; 8:74-77.
Dykes, 1999. Dykes EH: Paediatric trauma. Br J Anaesth 1999; 83:130-138.
Eddy et al., 1990. Eddy AC, Rusch VW, Fligner CL, et al: The epidemiology of traumatic rupture of the thoracic aorta in children: A 13-year review. J Trauma 1990; 30:989-991.discussion 991–982
Eichelberger, 1993. Eichelberger MR: Pediatric trauma: Prevention, acute care, rehabilitation, St. Louis, Mosby–Year Book, Inc., 1993.
Farling et al., 1989. Farling PA, Johnston JR, Coppel DL: Propofol infusion for sedation of patients with head injury in intensive care. A preliminary report. Anaesthesia 1989; 44:222-226.
Fiser, 1990. Fiser DH: Intraosseous infusion. N Engl J Med 1990; 322:1579-1581.
Furnival, 2001. Furnival RA: Controversies in pediatric thoracic and abdominal trauma. Clin Pediatr Emerg Med 2001; 2:48-62.
Goodwin and Robinson, 2000. Goodwin MW, Robinson KN: A pragmatic approach to fasting in paediatric trauma?. Paediatr Anaesth 2000; 10:452-453.
Green and Rothrock, 2002. Green SM, Rothrock SG: Is pediatric trauma really a surgical disease?. Ann Emerg Med 2002; 39:537-540.
Gupta et al., 1997. Gupta S, Heath K, Matta BF: Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans. Br J Anaesth 1997; 79:469-472.
Guy et al., 1993. Guy J, Haley K, Zuspan SJ: Use of intraosseous infusion in the pediatric trauma patient. J Pediatr Surg 1993; 28:158-161.
Haftel et al., 1988. Haftel AJ, Lev R, Mahour GH, et al: Abdominal CT scanning in pediatric blunt trauma. Ann Emerg Med 1988; 17:684-689.
Haller et al., 1994. Haller Jr JA, Papa P, Drugas G, Colombani P: Nonoperative management of solid organ injuries in children. Is it safe. Ann Surg 1994; 219:625-628.discussion 628–631
Hastings and Wood, 1994. Hastings RH, Wood PR: Head extension and laryngeal view during laryngoscopy with cervical spine stabilization maneuvers. Anesthesiology 1994; 80:825-831.
Hasue et al., 1974. Hasue M, Hoshino R, Omata S, et al: Cervical spine injuries in children. Fukushima J Med Sci 1974; 20:115-123.
Haughton et al., 1999. Haughton A, Turley A, Pollock N: Remifentanil for rapid sequence induction. Anaesth Intensive Care 1999; 27:319-320.
Hedequist et al., 1999. Hedequist D, Starr AJ, Wilson P, Walker J: Early versus delayed stabilization of pediatric femur fractures: Analysis of 387 patients. J Orthop Trauma 1999; 13:490-493.
Hellmann et al., 1993. Hellmann JR, Shott SR, Gootee MJ: Impalement injuries on the palate in children: Review of 131 cases. Int J Pediatr Otorhinolaryngol 1993; 26:157-163.
Herregods et al., 1988. Herregods L, Verbeke J, Rolly G, Colardyn F: Effect of propofol on elevated intracranial pressure. Preliminary results. Anaesthesia 1988; 43:107-109.
Imm and Carlson, 1993. Imm A, Carlson RW: Fluid resuscitation in circulatory short. Crit Care Clin 1993; 9:313-333.
Jaicks et al., 1997. Jaicks RR, Cohn SM, Moller BA: Early fracture fixation may be deleterious after head injury. J Trauma 1997; 42:1-5.discussion 5–6
Jean et al., 1998. Jean WC, Spellman SR, Nussbaum ES, Low WC: Reperfusion injury after focal cerebral ischemia: The role of inflammation and the therapeutic horizon. Neurosurgery 1998; 43:1382-1396.
Kaban, 1993. Kaban LB: Diagnosis and treatment of fractures of the facial bones in children. J Oral Maxillofac Surg 1993; 51:722-729.
Kalb et al., 1998. Kalb DC, Ney AL, Rodriguez JL, et al: Assessment of the relationship between timing of fixation of the fracture and secondary brain injury in patients with multiple trauma. Surgery 1998; 124:739-744.discussion 744–735
Karp et al., 1986. Karp MP, Jewett Jr TC, Kuhn JP, et al: The impact of computed tomography scanning on the child with renal trauma. J Pediatr Surg 1986; 21:617-623.
Kisa and Schenk, 1986. Kisa E, Schenk 3rd WG: Indications for emergency intravenous pyelography (IVP) in blunt abdominal trauma: A reappraisal. J Trauma 1986; 26:1086-1089.
Krantz, 1996. Krantz B: Initial assessment. In: Feliciano DV, Mattox KL, ed. Trauma, 5th ed.. Stamford: Appleton & Lang; 1996:123-129.
Kruskall et al., 1988. Kruskall MS, Mintz PD, Bergin JJ, et al: Transfusion therapy in emergency medicine. Ann Emerg Med 1988; 17:327-335.
Langer et al., 1989. Langer JC, Winthrop AL, Wesson DE, et al: Diagnosis and incidence of cardiac injury in children with blunt thoracic trauma. J Pediatr Surg 1989; 24:1091-1094.
Marcin and Pollack, 2002. Marcin JP, Pollack MM: Triage scoring systems, severity of illness measures, mortality prediction models in pediatric trauma. Crit Care Med 2002; 30:S457-S467.
Marion et al., 1997. Marion DW, Penrod LE, Keley SF, et al: Treatment of traumatic brain injury with moderate hyperthermia. N Engl J Med 1997; 336:540-546.
Marsaglia and Thomas, 1971. Marsaglia A, Thomas ED: Mathematical consideration of cross circulation and exchange transfusion. Transfusion 1971; 11:216-219.
Mayberg et al., 1995. Mayberg TS, Lam AM, Matta BF, et al: Ketamine does not increase cerebral blood flow velocity or intracranial pressure during isoflurane/nitrous oxide anesthesia in patients undergoing craniotomy. Anesth Analg 1995; 81:84-89.
McAninch and Carroll, 1988. McAninch JW, Carroll PR: Genitourinary trauma. In: Mattox KL, Moore EE, Feliciano DV, ed. Trauma, Norwalk: Appleton & Lange; 1988:537-552.
Mcheik et al., 2000. Mcheik JN, Vergnes P, Bondonny JM: Treatment of facial dog bite injuries in children: A retrospective study. J Pediatr Surg 2000; 35:580-583.
McKee et al., 1997. McKee MD, Schemitsch EH, Vincent LO, et al: The effect of a femoral fracture on concomitant closed head injury in patients with multiple injuries. J Trauma 1997; 42:1041-1045.
Mehall et al., 2001. Mehall JR, Ennis JS, Saltzman DA, et al: Prospective results of a standardized algorithm based on hemodynamic status for managing pediatric solid organ injury. J Am Coll Surg 2001; 193:347-353.
Melillo et al., 2001. Melillo EP, Hawkins DJ, Lynch L, Macnamara A: Difficult airway management of a child impaled through the neck. Paediatr Anaesth 2001; 11:615-617.
Mendelson et al., 2001. Mendelson SA, Dominick TS, Tyler-Kabara E, et al: Early versus late femoral fracture stabilization in multiply injured pediatric patients with closed head injury. J Pediatr Orthop 2001; 21:594-599.
Meyer, 1999. Meyer PG: Critical care management of severe paediatric trauma: A challenge for anaesthesiologists. Paediatr Anaesth 1999; 9:373-376.
Michaud et al., 1991. Michaud LJ, Rivara FP, Longstreth Jr WT, Grady MS: Elevated initial blood glucose levels and poor outcome following severe brain injuries in children. J Trauma 1991; 31:1356-1362.
Monkhoff et al., 2001. Monkhoff M, Schwarz U, Gerber A, et al: The effects of sevoflurane and halothane anesthesia on cerebral blood flow velocity in children. Anesth Analg 2001; 92:891-896.
Mooney, 2002. Mooney DP: Multiple trauma: Liver and spleen injury. Curr Opin Pediatr 2002; 14:482-485.
Morell et al., 1997. Morell RC, Colonna DM, Mathes DD, Wilson JA: Fluoroscopy-assisted intubation of a child with an unstable subluxation of c1/cJ2. Neurosurg Anesthesiol 1997; 9:25-28.
Moriarty et al., 1997. Moriarty KP, Harris BH, Benitez-Marchand K: Carotid artery thrombosis and stroke after blunt pharyngeal injury. J Trauma Injury Infect Crit Care 1997; 42:541-543.
Morrison et al., 2002. Morrison W, Wright JL, Paidas CN: Pediatric trauma systems. Crit Care Med 2002; 30:S448-S456.
Musgrave and Mendelson, 2002. Musgrave DS, Mendelson SA: Pediatric orthopedic trauma: Principles in management. Crit Care Med 2002; 30:S431-S443.
Nakayama et al., 1990. Nakayama DK, Gardner MJ, Rowe MI: Emergency endotracheal intubation in pediatric trauma. Ann Surg 1990; 211:218-223.
Nakayama et al., 1989. Nakayama DK, Ramenofsky ML, Rowe MI: Chest injuries in childhood. Ann Surg 1989; 210:770-775.
Nakayama et al., 1992. Nakayama DK, Waggoner T, Venkataraman ST, et al: The use of drugs in emergency airway management in pediatric trauma. Ann Surg 1992; 216:205-211.
Niemi and Kuitunen, 1998. Niemi TT, Kuitunen AH: Hydroxyethyl starch impairs in vitro coagulation. Acta Anaesthesiol Scand 1998; 42:1104-1109.
Olsson et al., 1986. Olsson GL, Hallen B, Hambraeus-Jonzon K: Aspiration during anaesthesia: A computer-aided study of 185,358 anaesthetics. Acta Anaesthesiol Scand 1986; 30:84-92.
Pinaud et al., 1990. Pinaud M, Lelausque JN, Chetanneau A, et al: Effects of propofol on cerebral hemodynamics and metabolism in patients with brain trauma. Anesthesiology 1990; 73:404-409.
Potola et al., 2000. Potoka DA, Schall LC, Gardner MJ, et al: Impact of pediatric trauma centers on mortality in a statewide system. J Trauma 2000; 49:237-245.
Rasmussen and Grande, 1994. Rasmussen GE, Grande CM: Blood, fluids, and electrolytes in the pediatric trauma patient. Int Anesthesiol Clin 1994; 32:79-101.
Ravussin et al., 1988. Ravussin P, Guinard JP, Ralley F, Thorin D: Effect of propofol on cerebrospinal fluid pressure and cerebral perfusion pressure in patients undergoing craniotomy. Anaesthesia 1988; 43:37-41.
Rhodes, 1998. Rhodes M: Trauma resuscitation. In: Peitzman AB, Rhodes M, Schwab CW, Yealy DM, ed. The trauma manual, Philadelphia: Lippincott-Raven; 1998:82-90.
Rielly et al., 1993. Rielly JP, Brandt ML, Mattox KL, Pokorny WJ: Thoracic trauma in children. J Trauma 1993; 34:329-331.
Rizoli, 2003. Rizoli SB: Crystalloids and colloids in trauma resuscitation: A brief overview of the current debate. J Trauma 2003; 54:S82-S88.
Roback, 2000. Roback MG: America's tragedy: Pediatric trauma. Emerg Med Serv 2000; 29:61-65.
Rosetti et al., 1985. Rosetti VA, Thompson BM, Miller J, et al: Intraosseous infusion: An alternative route of pediatric intravascular access. Ann Emerg Med 1985; 14:885-888.
Schwab et al., 1986. Schwab CW, Shayne JP, Turner J: Immediate trauma resuscitation with type O uncrossmatched blood: A two-year prospective experience. J Trauma 1986; 26:897-902.
Shaikh and Worrall, 2002. Shaikh ZS, Worrall SF: Epidemiology of facial trauma in a sample of patients aged 1–18 years. Injury 2002; 33:669-671.
Shiozaki et al., 1999. Shiozaki T, Kato A, Taneda M, et al: Little benefit from mild hypothermia therapy for severely head injured patients with low intracranial pressure. J Neurosurg 1999; 91:185-191.
Smith, 2001. Smith GACommittee on Injury and Poison Prevention: Technical report: lawnmower-related injuries to children. Pediatrics 2001; 107:E106.
Solheim and Wesenberg, 2001. Solheim BG, Wesenberg F: Rational use of blood products. Eur J Cancer 2001; 37:2421-2425.discussion 2425–2427
Spitzfaden et al., 1999. Spitzfaden AC, Jimenez DF, Tobias JD: Propofol for sedation and control of intracranial pressure in children. Pediatr Neurosurg 1999; 31:194-200.
Stafford et al., 2002. Stafford PW, Blinman TA, Nance ML: Practical points in evaluation and resuscitation of the injured child. Surg Clin North Am 2002; 82:273-301.
Stewart et al., 1994. Stewart L, Bullock R, Rafferty C, et al: Propofol sedation in severe head injury fails to control high ICP, but reduces brain metabolism. Acta Neurochir Suppl 1994; 60:544-546.
Stowe et al., 1992. Stowe DF, Bosnjak ZJ, Kampine JP: Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts. Anesth Analg 1992; 74:547-558.
Swischuk, 1986. Swischuk LE: The spine and spinal cord: Emergency radiology of the acutely ill or injured child, Baltimore, Williams & Wilkins, 1986.
Teasdale and Jennett, 1974. Teasdale G, Jennett B: Assessment of coma and impaired consciousness: A practical scale. Lancet 1974; 2:81-84.
Tepas et al., 1990. Tepas 3rd JJ, DiScala C, Ramenofsky ML, Barlow B: Mortality and head injury: The pediatric perspective. J Pediatr Surg 1990; 25:92-95.discussion 96
Tepas et al., 2003. Tepas 3rd JJ, Frykberg ER, Schinco MA, et al: Pediatric trauma is very much a surgical disease. Ann Surg 2003; 237:775-780.
Tobias, 1994. Tobias JD: Increased intracranial pressure after fentanyl administration in a child with closed head trauma. Pediatr Emerg Care 1994; 10:89-90.
Townsend et al., 1998. Townsend RN, Lheureau T, Protech J, et al: Timing fracture repair in patients with severe brain injury (Glasgow Coma Scale score <9). J Trauma 1998; 44:977-982.
US Consumer Product Safety Commission, 1990-1999. US Consumer Product Safety Commission : National Electronic Injury Surveillance System (Database), Bethesda, MD, US Consumer Product Safety Commission, 1990-1999.
Vane, 2002. Vane DW: Imaging of the injured child: Important questions answered quickly and correctly. Surg Clin North Am 2002; 82:315-323.
Vavilala and Lam, 2002. Vavilala MS, Lam AM: Perioperative considerations in pediatric traumatic brain injury. Int Anesthesiol Clin 2002; 40:69-87.
Ward, 1995. Ward JD: Craniocerebral injuries. In: Buntain WL, ed. Management of pediatric trauma, Philadelphia: WB Saunders; 1995:177-188.
Watts et al., 1997. Watts AD, Gelb AW, Bach DB, Pelz DM: Comparison of the Bullard and Macintosh laryngoscopes for endotracheal intubation of patients with a potential cervical spine injury. Anesthesiology Dec 1997; 87(6):1335-1342.
Waxman et al., 1980. Waxman K, Shoemaker WC, Lippmann M: Cardiovascular effects of anesthetic induction with ketamine. Anesth Analg 1980; 59:355-358.
Zanette et al., 1997. Zanette G, Ori C, Zadra N, et al: Hangman's fracture in a paediatric patient: Considerations for anaesthesia. Paediatr Anaesth 1997; 7:473-475.
Zerfowski and Bremerich, 1998. Zerfowski M, Bremerich A: Facial trauma in children and adolescents. Clin Oral Invest 1998; 2:120-124.