Trauma Pediatric - part 6 pot

27. Sessler DI. Perioperative thermoregulation and heat balance. Ann New York Acad Sci 1997; 813:757–777. 28. Handrigan MT, Wright RO, Becker BM, Linakis JG, Jay GD. Factors and methodology in achieving ideal delivery temperatures for intravenous and lavage fluid in hypothermia. Am J Emerg Med 1997; 15(4):350–353. 29. Bernardo LM, Henker R, Bove M, Sereika S. The effect of administered crystalloid fluid temperature on aural temperature of moderately and severely injured children. J Emerg Nursing Online 1997; 23(2). 30. Sieunarine K, White G. Full thickness burn and venous thrombosis following intrave- nous infusion of microwave heated crystalloid fluids. Burns 1996; 22(7):568–569. 31. Neville H, Lally K, Cox C. Emergent abdominal decompression with patch abdomino- plasty in the pediatric patient. J Pediat Surg 2000; 35(5):705–708. 32. DeCou JM, Abrams RS, Miller RS, Gauderer MWL. Abdominal compartment syn- drome in children: experience with three cases. J Pediat Surg 2000; 35(6):840–842. 33. Waisman D, Shupak A, Weisz G, Melamed Y. Hyperbaric oxygen therapy in the pedia- tric patient: the experience of the Israel Naval Medical Institute. Pediatrics 1998; 102(5):e53. 34. Iskit SH, Alpay H, Tugtepe H, Ozdemir C, Ayyildiz S, Ozel K, Imamoglu S, Cabukoglu S, Tetik. Analysis of 33 pediatric trauma victims in the 1999 Marmara earthquake, in British Association of Pediatric Surgeons 17th Annual International Congress, Sorrento, Italy, 2000. 35. Partrick DA, Bensard DD, Moore EE, Partington MD, Karrer FM. Driveway crush injuries in young children: a highly lethal, devastating, and potentially preventable event. J Pediat Surg 1998; 33(11):1712–1715. 36. McLean DE, Kearney J, Cawley MF. Environmental responsive temperature instability in pediatric spinal cord injury. Spinal Cord 1999; 37:705–709. 37. Capron AM. Brain death— well settled yet still unresolved Editorial. N Engl J Med 2001; 344(15):1244–1246. 38. Wijdicks EFM, The diagnosis of brain death. N Engl J Med 2001; 344(16):1215–1221. 39. Metz J, McGrath KM, Copperchini ML, Haeusler M, Haysom HE, Gibson PR, Millar RJ, Babarczy A, Ferris L, Grigg AP. Appropriateness of transfusions of red cells, plate- lets and fresh frozen plasma. An audit in a tertiary care teaching hospital. Med J Aust 1995; 162(11):572–577. 40. Steiner RB, Adolph VR, Heaton JF, Bonis SL, Falterman KW, Arensman RM. Pediatric extracorporeal membrane oxygenation in posttraumatic respiratory failure. J Pediat Surg 1991; 26(9):1011–1015. 41. Bunchman TE. Pediatric hemodialysis: lessons from the past, ideas for the future. Kidney Int 1996; 49(Suppl 53):s64–s67. 42. Brandt ML, Nuchtern JG, Brewer ED. Suggestions for placing an initial vascular access for hemodialysis in children. Contemp dial nephrol 1997; (September):26–29. 43. Reznik VM, Griswold WR, Peterson BM, Rodarte A, Ferris ME, Mendoza SA. Perito- neal dialysis for acute renal failure in children. Pediatr Nephrol 1991; 5:715–717. 44. Jeschke MG, Barrow RE, Herndon DN. Recombinant human growth hormone treat- ment in pediatric burn patients and its role during the hepatic acute phase response. Cri- tical Care Med 2000; 28(5):1578–1584. 45. Moore FA, Feliciano DV, Andrassy RJ, McArdle AH, Booth FV, Morgenstein-Wagner TB, Kellum JM Jr, Welling RE, Moore EE. Early enteral feeding, compared with parent- eral, reduces postoperative septic complications. The results of a meta-analysis. Ann Surg 1992; 216:172–183. 46. Weimann A, Bastian L, Bischoff WE, Grotz M, Hansel M, Lotz J, Trautwein C, Tusch G, Schlitt HJ, Regel G. Influence of arginine, omega-3 fatty acids and nucleo- tide-supplemented enteral support on systemic inflammatory response syndrome and multiple organ failure in patients after severe trauma. Nutrition 1998; 14(2):165–172. 208 Dilley and Wesson 47. Borzotta AP, Pennings J, Papasadero B, Paxton J, Mardesic S, Borzotta R, Parrott A, Bledsoe F. Enteral versus parenteral nutrition after severe closed head injury. J Trauma 1994; 37(3):459–468. 48. Shew SB, Jaksic T. The metabolic needs of critically ill children and neonates. Sem Pediatr Surg 1999; 8(3):131–139. 49. Windsor JA, Hammodat H. Metabolic management of severe acute pancreatitis. World J Surg 2000; 24(6):664–672. 50. Rattner DW, Legermate DA, Lee MJ, Mueller PR, Warshaw AL. Early surgical debride- ment of symptomatic pancreatic necrosis is beneficial irrespective of infection. Am J Surg 1992; 163(1):105–110. 51. Fernandez-del Castillo C, Rattner DW, Makary MA, Mostafavi A, McGrath D, War- shaw AL. Debridement and closed packing for the treatment of necrotizing pancreatitis. Ann Surg 1999; 230(4):676–684. Pediatric Organ Failure 209 15 Treatment of Severe Pediatric Head Injury: Evidence-Based Practice Jodi L. Smith Pediatric Neurosurgery, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, Indiana, U.S.A. INTRODUCTION Head injury is a leading cause of death and acquired disability in the pediatric population. Despite this, data from well-designed clinical studies, which could be used to guide the management of children with severe traumatic brain injury, are scarce. Most of the randomized controlled trials designed to evaluate head injury have excluded pediatric patients. Because of the paucity of proven therapies in pediatric head injury, management stra tegies for severely head-injured children are generally extrapolated from adult studies. Because pediatric patients are not simply small adults, therapy should be based on scientific evidence that a particular type of treatment will actually improve a child’s outcome from traumatic brain injury. Many of the therapies that are routinely employed in the treatment of adults with severe head injury have not been tested in randomized controlled trials. In fact, management strategies in the care of patients of all ages have relied in large part on expert opinion and practice experience. This has resulted in tremendous variations in the treatment and outcomes of head-injured patients, with mortality rates ranging from 25% to 60%. In an attempt to standardize the care of patients with severe head injury and ultimately improve outcome, the American Association of Neurological Surgeons and the Brain Trauma Foundation performed a thorough review of the existing head injury literature and developed evidence-based standards, guidelines, and treatment options for managing adult patients with severe head injury (1). These guidelines were designed to provide uniform practice parameters to prevent or mini- mize brain swelling (and the irreversible damage that occurs from this swelling) and to create and maintain a physiologic environment to maximize brain recovery. The following topics , which were deemed to have an impact on the outcome of patients with severe head injury, were addressed in this publication:  early resuscitation,  intracranial pressure (ICP) monitoring,  ICP treatment threshold and methods,  use of mannitol, barbiturates, nutrition, hyperventilation, corticosteroids, and prophylactic anticonvulsants in the treatment of head injury. PART III: SPECIFI C INJURIES 211 For mo st of the clinical practice parameters addressed in this publication, there were insufficient data to support a treatment standard. In fact, based on an analysis of all the available data, there were only three ‘‘standards of clinical care’’ for the treatment of severe he ad injury in adult patients. These included: 1. the avoidance of steroids for treating elevated ICP, 2. the avoidance of routine use of prolonged hyperventilation, 3. the avoidance of prophylactic anticonvulsants for the prevention of late post-traumatic seizures. Focused, well-designed, and carefully implemented clinical research trials are required to upgrade clinical practice parameters to treatment standards. Despite the fact that traumatic brain injuries are more c ommon in pediatric trauma than in adult trauma, no specific recommendations were made in the adult guidelines regarding the treatment of traumatic brain injury in p ediatric patients. A subsequent meticulous analysis of this publication for relevance to the manage- ment of severe pedia tric head injury revealed even fewer recommendations for standardsofcare(2).Inanattempttostandardizeandimprovetreatmentpractice and patient outcome in pediatric patients with severe head injury, a multidisciplin- ary team of clinicians and researchers recently review ed all the available data o n this topic and subsequently publi shed evidence-base d practice standards, guide- lines, and treatment options for the acute medical management of pediatric patients with severe traumatic brain injury (3). In the pediatric guidelines as in the adult guidelines practice standards refer to accepted principles of patient man- agement that reflect a high degree of clinical certainty (i.e., they are based predominantlyonclassIdata,derivedfromrandomizedcontrolledtrials,aswell as on som e strong class II data, derived mainly from prospective and some retro- spective studies) (1,3). In addition, practice guidelines refer to management strate- gies that reflect a moderate degree of clinical certainty (i.e., they are based on classes II and III data, derived from retrospective studies such as clinical series, case reports, expert opinions, and databases or registries). Finally, treatment options refer to management strategies for which the cli nical certainty is unclear (i.e., they are based solely on class II I data or represent the consensus of experts in areas where studies d ocumenting more definitive levels of certainty are not avail- able or are not possible). Be sides elucidating scientific evidence that supports var- ious treatment strategies and the rigor of the evidence, this analysis on the treatment of severe pediatric head injury revealed that pediatric head injury is under investi gated and that many questions remain unanswered, especially at the class I level, re garding the optimal medical and surgical management o f seve re traumatic brain injury in the pediatric population (3). Thus, large, well- designed, prospective, randomized, controlled multicenter trials are still needed to investigate additional treatment modalities and provide standards of care for the management of severe pediatric h ead injury. The present chapter discusses current therapeutic options for the management of severe head injury in pediatric patients. Aspects of care covered in this chapter include both prehospital and intens ive management of pediatric patients with severe head injury. The management strategies described herein are based on existing scien- tific evidence and include recommendations from the recently published evidence- based pediatric guidelines (3). In this chapter, pediatric patients refer to patients who are 17 years of age or younger; severe head injury is defined using the Glasgow Coma 212 Smith Scale with a score eq ual to or less than eight; and traumatic brain injury includes both accidental and non-acci dental causes (4). PATHOPHYSIOLOGY OF HEAD INJURY Before proceeding with a discussion on evidence-based management strategies for the treatment of severe pediatric head injury, it is first necessary to review the patho- physiology of head injury. Severe traumatic brain injury involves two types of injury—primary and secondary. Primary injury arises at the time of the traumatic event and generates the initial damage that occurs at the moment of impac t, includ- ing structural damage to neurons, supporting tissues, and blood vessels. Examples of primary injury include skull fracture, epidural and subdural hematomas, intrapar- enchymal hemorrhage, cortical contusions, diffuse axonal injury, and brain stem injury. In contrast, secondary injury is an evolving process that develops during the hours and days that follow the initial trauma and produces additional progres- sive cellular damage and dysfunction resul ting from degenerative biochemical pro- cesses initiated both by the primary injury and by additional systemic insults such as hypotension and hypoxia. Secondary injury, which compounds the primary injury, occurs as a consequence of brain swelling (from acute cerebral arterial vaso- dilatation and associated increased cerebral blood volume), diffuse cerebral edema (from increased cerebral water content), elevated ICP, cerebral herniation, traumatic ischemia and/or infarction, secondary hemorrhage, hypotension, and hypoxia. Thus, only part of the damage to the brain that occurs during head trauma takes place at the moment of impact. The main goal of acute management of severe head trauma is to minimize the progression or the effects of secondary injury and thereby maximize the potential for recovery. Successful management of severe pediatric head injury requires complete and rapid physiologic resuscitation, prevention of hypotension and hypoxia, treatment of elevated ICP, and maintenance of cerebral perfusion to facilitate adequate delivery of oxygen and metabolic substrates to the brain. The developing/maturing brain of a child undergoes changes that affect its susceptibility to both primary and secondary injury. For example, children have less cerebrospinal fluid volume, which results in less buffering capacity for changes in intracranial tissue volume and places them at risk for earlier decompensation and secondary ischemia after traumatic brain injur y. Open fontanels and expandable calvarial sutures do not add buffering capacity and, therefore, are not protective in head-injured infants. Because of these and many other differences that exist between pediatric and adult patients, the treatment of head injury in the pediatric population should not be based on generalizations from studies in adults but rather should rely on scientific evidence derived from studies on pediatric patients. The remainder of this chapter focuses on evidence-based management strategies for the treatment of severe pe diatric he ad injury. EVIDENCE-BASED TREATMENT STRATEGIES— PRE-HOSPITAL CARE Speed of access to definitive care and timing of the intervention relative to the initial insult play a paramount role in the survival and eventual outcome of pediatric pati- ents with severe head injury. In support of this, several studies have reported a Treatment of Severe Pediatric Head Injury 213 decreased mortality rate in severely head-in jured pediatric patients treated in pediatric trauma centers (5–8). However, as pointed out in the recently establ ished pediatric guidelines transfer did not improve the survival of some subgroups (3). For example, patients in rural areas who were taken initially to Levels III and IV rural hospitals then transferred to a higher level of care, had a significantly increa sed mortality rate (9). The results of this study suggest that severely head-injured pedia- tric patients are more likely to survive if they are transported directly to a Level I or II pediatric trauma center than if transported first to another type of trauma center and then transferred to a pediatric trauma center. Based on this, the followi ng recommendations were made in the ped iatric guidelines (3): 1. Pediatric patients with severe traumatic bra in injury should be transported directly to and treated in a pediatric trauma center if available (guideline) or to an adult trauma center staffed with qualified, pediatric-trained caregivers and equipment necessary for treating pediatric patients if no pediatric trauma center is available (option). 2. Although the literature provides strong evidence to support a role for trauma systems and pediatric trauma centers in the increased survival of pediatric patients with severe head injury, their role on the eventual func- tional outcome of pediatric patients with severe head injury remains unclear. Airway Management Hypoxemia, which commonly occurs during the prehospital care of severely head- injured children is associated with poorer functional outcomes in pediatric patients with traumatic brain injury (10–13). Despite this, evidence suggesting that aggressive prehospital airway management (i.e., endotracheal intubation over bag-valve-mask ventilation) improves outcome for children with traumatic brain injury is lacking (14). The pediatric guidelines make two recommendations regarding the prehospital management of airway in severely head-injured pediatric patients (3): 1. Avoid hypoxia if possible or correct it immediately by administering supp- lemental oxygen (guideline), 2. Perform endotracheal intubation in the prehospital setting guided by end- tidal CO 2 detectors and only by scene-critical care providers who are speci- fically trained to intubate pediatric patients (option). If qualified caregivers are unavailable, then bag-valve-mask ventilation should be carried out until the patient reaches a traum a center staffed with the appropriately trained personnel in order to prevent lif e-threatening complications directly related to attempts at intubation by unqualified scene-critical care providers. Management of Breathing and Circulation In addition to the initial damage that occurs within the brain at the moment of impact, progressive cellular damage and dysfunction frequently occur in the ensuing hours and days as a consequence of degenerative biochemical processes initiated both by the primary injury and by additional systemic insults such as hypotension and hypoxia. Because of the exquisite sensitivity of the injured brain to secondary systemic and local intracranial insults, they must be avoided in order to minimize the progression of brain injury and maximize the potential for recovery (15–21). 214 Smith Hypotension and hypoxia, which commonly occur in pediatric patients with severe traumatic brain injury, have the greatest negative impact on outcome, includ- ing increased morbidity and mortality (12,17,22–27). For example, in a prospective study of 200 pediatric patients the mortality rate was significantly higher in the pre- sence of hypotension, hypoxia, or hypercarbia than it was in the absence of these fac- tors (i.e., 55% vs. 7.7% , p < 0.01) (23). In another study analyzing the influence of hypoxia and hypotension on mortality from severe traumatic brain injury in children hypotension on admission was associated with a mortality rate of 61%, which increased to 85% when both hypotension and hypoxia were present, compared with only 22% when patients were normotensive on admission (17). Finally, in a prospec- tive analysis of severe traumatic brain injury in 6908 adults and 1906 children younger than 15 years of age at 41 trauma centers, hypotension was associated with significantly higher mortality rates in children and had a more harmful effect in chil- dren than in adults (25). Hypotension in children is defined as systolic blood pressure below the fifth percentile for age or by clinical signs of shock. The lower limit of systolic blood pres- sure for age (i.e., the fifth percentile) can be estimated by multiplying the patient’s age in years by two, and then by adding this number to 70 mmHg (28). Because pediatric patients can maintain their blood pressure in the face of significant volume depletion and clinical signs of shock, it is imperati ve that the pediatric traumatic brain injury patient be monitored closely for signs of decreased perfusion, including tachycardia, urine output less than 1 mL/kg/hr, or capillary filling time great er than two seconds. Patients who exhibit such signs, even in the face of a normal blood pressure, undergo adequate resuscitation with intravenous fluids. In addition, hypo- tensive patients or those showing signs of decreased perfusion should undergo a thorough evaluation for extracranial sources of hypotension, including internal bleeding or spinal cord injury, and the source(s) should be corrected as rapidly as possible. Finally, there is no role for fluid restriction in the management of severely head-injured pediatric patients demonstrating clinical signs of shock (29). Hypoxia in children is defined as PaO 2 <60–65 mmHg, oxygen saturation <90%, apnea, or cyanosis. Hypoventilation, which results in hypercarbia, is defined as ineffective respiratory rate for age, shallow or irregular respirations, frequent epi- sodes of apnea, or measured hypercarbia. Hypoxia and hypo ventilation commonly occur in pediatric patients after severe traumatic brain injury and can have a nega- tive impact on mortality rate and the severity of disability of survivors (22,23). Hence, it is important to obtain early airway control and to use assisted ventilation with 100% oxygen as needed in the resuscitation phase of care to avoid hypoxia and hypercarbia. Moreover, it is essential to perform continuous monitoring of oxygena- tion and ventilation to avoid hypoxia and hypercarbia or to detect and correct them as rapidly as possible to age-appropriate parameters. As with all other critically injured pediatric patients, the prehospital manage- ment (i.e., in the field and during transport) of pediatric patients with severe traumatic brain injury is of paramount importance and must be optimized in order optimize outcome. The goal of such man agement is to prevent secondary brain injury by obtaining early airway control and restoring oxygenation, ventilation, circulating blood volume, and blood pressur e (i.e., the ABCs of resuscitation). Based on previous studies (12,17,22–27), the followin g recommendations were made in the pediatric guidelines (3). Treatment guidelines included recognizing and correcting hypotension as rapidly as possible with intravenous fluids and evaluating and treat- ing all associated extracranial injuries. Treatment options included: Treatment of Severe Pediatric Head Injury 215 1. obtaining airway control in children with a Glasgow Coma Score 8orin the face of hypoventilation, 2. using assisted venti lation and 100% oxygen during the resuscitation phase of care in order to prevent hypoxemia, hypercarbia, and aspiration, 3. performing continuous assessment of oxygenation and ventilation using pulse oximetry and end-tidal CO 2 monitoring and/or serial arterial blood gas measurements, 4. recognizing and correcting hypoxia as rapidly as possible, 5. monitoring blood pressure frequently and administering intravenous fluids as needed to maintain systolic blood pressure within the normal range for age. In addition, although there are no pediatric studies to date that evaluate the effect of brain-directed therapies in the prehospital setting, such as the use of seda- tion, analgesia, neuromuscular blockade, mannit ol, hypertonic saline, or hyperven- tilation, on the outcome from severe pediatric traumatic brain injury, the pediatric guidelines made the following recommendations regarding the use of these thera- pies (3). Specifically, they recommended as a treatment option the prehospital use of sedation, analges ia, and neu romuscular blockade to optimize transport of the pedia- tric patient with traumatic brain injury. However, they recommended against the prophylactic use of mannitol and hyperventilation (i.e., 25 breaths per minute in a child and 30 breaths per minute in an infant) in pediatric patients with traumatic brain injury in the prehospital setting except in euvolemic, normotensive patients exhibiting definite signs of cerebral herniation, or acute neurologic deterioration. The prehospital prophylactic use of brain-directed therapi es, such as mannitol and hypertension, is not recommended because these treatment modalities can exacer- bate intracranial ischemia and interfere with resuscitation. Finally, as pointed out in the pediatric guidelines although previous studies have shown that hypotension and hypoxia are potentially avoidable secondary insults that significantly increase the morbidity and mortality of severe pediatric traumatic brain injury patients, evidence suggesting that outcome from severe head injury is improved by preventing hypotension and hypoxia in the prehospital setting is lacking (3). Further studies are needed in pediatric patients with severe head injury to assess the role of prehospital hypotension and hypoxia on functional outcome, to ascertain treatment thresholds for hypotension and hypoxia, to evaluate the potential beneficial role of hyperten- sion, and to assess prehospital management protocols, including brain-directed therapies, in order to optimize prehospital management and subsequent functional outcome of pediatric patients with severe head injury. EVIDENCE-BASED TREATMENT STRATEGIES— INTENSIVE MANAGEMENT The use of intensive management protocols has significantly reduced mortality and morbidity in pediatric patients with severe head injury. Such protocols include early intubation and rapid transport to an appropriate trauma care facility; prompt intra- venous fluid resuscitation; CT scanning; surgical evacuation of intracranial mass lesions; and meticulous management in an intensive care unit setting, with continuous monitoring of physiologic parameters. Routine monitoring of pediatric patients with severe head injury includes continuous invasive arterial blood pressure monitoring, 216 Smith pulse oximetry, and monitoring of ICP, central venous pressure, temperature, end-tidal carbon dioxide, and urine output. The primary goal of intensive management of severe pediatric head injury is to improve mortality rates and functional recovery by prevent- ing secondary injury to the brain caused by systemic hypotension, hypoxia, elevated ICP, and/or reduced cerebral perfusion pressure (CPP). To avoid secondary brain injury, normal, age-appropriate physiologic parameters must be maintained or prompt intervention must occur when deviations in these parameters arise. The CPP, defined as the mean arterial bloo d pressure (MAP) minus ICP, is the physiologic variable that represents the pressure gradient driving cerebral blood flow and metabolite/oxygen delivery and, therefore, is related to cerebral ischemia. The harmful consequences of elevated ICP stem from its effect on regional and global cerebral blood flow. Pediatric patients with severe traum atic brain injury, especially those with subdural hematomas, large multifocal contusions, hypoxic injury, and/or gunshot wounds to the head, frequently develop significant brain swelling and/or diffuse cerebral edema, whi ch, in turn, cause intracranial hypertension (i.e., patholo- gically elevated ICP) and a reduction in cerebral blood flow (i.e., cerebral ischemia). Because intracranial hypertension is associated with decreased survival and poor functional outcome, pediatric patients with severe head injury require aggressive monitoring in the pediatric intens ive care unit, including ICP monitoring, to enable rapid detection and correction of neurologic deterioration through medical an d/or surgical treatment. Intracranial Pressure Monitoring Although to date no randomized controlled clinical trial exists that examines the role of ICP monitoring on the functional outcome of pediatric patients with severe trau- matic brain injury, ICP monitoring and the medical and/or surgical treatment of intracranial hypertension are mainstays in the management of severe pediatric head injury and have become widely accepted practice. Maintenance of physiologic ICP is necessary to ensure adequate cerebral perfusion, which, in turn, is required for the delivery of oxygen and metabolic substrates to neurons and supporting cells. In addi- tion, phy siologic ICP must be maintained to prevent cerebral herniations (caused by the mechanical displacement of brain, cerebrospinal fluid, and blood vessels from one cranial compartment to another) and subsequent cerebral infarction. Several class III studies pro vide evidence to support an association between intracranial hypertension and poor neurologic outcome (22,30–32). Moreover, other class III studies provide strong evidence that accurat e continuous monitoring of ICP with effective treatment of elevated ICP in severely head-injured pediatric patients results in improved functional outco mes (33–36). Therefore, in pediatric patients with severe head injury (i.e., GCS score 8 including infants), an ICP monitor should be placed for continuous ICP monitoring and treatment of elevated ICP in an intensive care unit setting, especially in the face of diffuse brain swelling, cisternal effacement, midline shift, and/or multiple contusions on the admitting head CT scan. In addition, the pediatric guidelines recommend at the option level that an ICP monitor may be placed in patients with a GCS >8 if a mass lesion is present or if serial neurologic examinations cannot be performed because of sedation, neuromuscular blockade, or anesthesia for management of extra cranial injuries (3). The goal of ICP management is to reduce the ICP enough to ensure an adequate supply of well-oxygenated blood to the brain. With regard to the recom- mended ICP level for which treatment should be initiated in pediatric patients with Treatment of Severe Pediatric Head Injury 217 [...]... blunt trauma is best at a pediatric trauma center J Pediatr Surg 19 96; 1:72–77 6 Hulka F, Mullins RJ, Mann NC, Hedges JR, Rowland D, Worrall WH, Sandoval RD, Zechnich A, Trunkey DD Influence of a statewide trauma system on pediatric hospitalization and outcome J Trauma 1997; 42:514–519 7 Johnson DL, Krishnamurthy S Send severely head-injured children to a pediatric trauma center Pediatr Neurosurg 19 96; ... patients (62 ,63 ) However, more recent studies have revealed that increased post-traumatic cerebral blood flow (i.e., hyperemia) is not a common finding after severe pediatric head injury and have raised concerns similar to those in the adult head-injury literature regarding ischemia from hyperventilation-induced vasoconstriction as a cause of secondary brain injury and worsened neurologic outcome (64 ,65 ) As... pressure and survival in pediatric brain-injured patients J Trauma 2000; 49 :65 4 65 9 33 Taylor A, Butt W, Rosenfeld J, Shann F, Ditchfield M, Lewis E, Klug G, Wallace D, Henning R, Tibballs J A randomized trial of very early decompressive craniectomy in Treatment of Severe Pediatric Head Injury 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 227 children with traumatic brain injury and... controlled clinical trial Acta Neurochir 1984; 72:157– 166 61 Ghajar J, Hariri RJ, Narayan RK, lacono LA, Firlik K, Patterson RH Survey of critical care management of comatose, head-injured patients in the United States Crit Care Med 1995; 23: 560 – 567 62 Schut L, Bruce DA Recent advances in the treatment of head injuries Pediatr Ann 19 76; 10:81–104 63 Bruce DA, Raphaely RC, Goldberg AI, Zimmerman RA, Bilaniuk... C Bicycle-related injuries among preschool children Ann Emerg Med 1997; 30: 260 4 Acton CH, Nixon JW, Clark RC Bicycle riding and oral/maxillofacial trauma in young children Med J Aust 19 96; 27: 165 5 Levine DA, Platt SL, Foltin GL Scooter injuries in children Pediatrics 2001; 107:E64 6 Shorter NA, Mooney DP, Harmon BJ Snowboarding injuries in children and adolescents Am J Emerg Med 1999; 17: 261 7 Shorter... injury in children Childs Brain 1979; 5:174–191 64 Zwienenberg M, Muizelaar JP Severe pediatric head injury: The role of hyperemia revisited J Neurotrauma 1999; 16: 937–943 65 Skippen P, Seear M, Poskitt K, Kestle J, Cochrane D, Annich G, Handel J Effect of hyperventilation on regional cerebral blood flow in head-injured children Crit Care Med 1997; 25:1402–1409 66 Polin RS, Shaffrey ME, Bogaev CA, Tisdale... AB, Yurkewicz L Clinical Trials in Head Injury J Neurotrauma 2002; 19:503–557 68 Fanconi S, Kloti J, Meuli M, Zaugg H, Zachmann M Dexamethasone therapy and endogenous cortisol production in severe pediatric head injury Intensive Care Med 1988; 14: 163 – 166 69 Kloti J, Fanconi S, Zachmann M, Zaugg H Dexamethasone therapy and cortisol excretion in severe pediatric head injury Childs Nerv Syst 1987; 3:103–105... Neurosurgery 2000; 46: 335–342 16 Pediatric Facial Trauma Barry L Eppley Indiana University School of Medicine, Indianapolis, Indiana, U.S.A INTRODUCTION Pediatric facial trauma patients differ from adults with similar injuries in several ways First, the pediatric patient has the advantage of an accelerated ability to heal with a minimum of complications, especially in the well-vascularized tissues... advantages, certain characteristics of the pediatric facial trauma patient must be kept in mind These include the anatomy of the immature face, the facial injury patterns from mechanisms typical of the pediatric patient, and the potential effect of trauma on growth, which makes long-term follow-up of these patients mandatory Because of these factors, children with facial trauma cannot be managed in the same... Potoka DA, Schall LC, Gardner MJ, Stafford PW, Peitzman AB, Ford HR Impact of pediatric trauma centers on mortality in a statewide system J Trauma 2000; 49:237–245 9 Clay Mann N, Mullins RJ, Hedges JR, Rowland D, Arthur M, Zechnich AD Mortality among seriously injured patients treated in remote rural trauma centers before and after implementation of a statewide trauma system Med Care 2001; 39 :64 3 65 3 . pancreatitis. Ann Surg 1999; 230(4) :67 6 68 4. Pediatric Organ Failure 209 15 Treatment of Severe Pediatric Head Injury: Evidence-Based Practice Jodi L. Smith Pediatric Neurosurgery, James Whitcomb. a statewide trauma system on pediatric hospita- lization and outcome. J Trauma 1997; 42:514–519. 7. Johnson DL, Krishnamurthy S. Send severely head-injured children to a pediatric trauma center intrave- nous infusion of microwave heated crystalloid fluids. Burns 19 96; 22(7): 568 – 569 . 31. Neville H, Lally K, Cox C. Emergent abdominal decompression with patch abdomino- plasty in the pediatric