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The Journal of Emergency Medicine, Vol. 37, No. 1, pp. 63–68, 2009Copyright © 2009 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/09 $–see front matter

doi:10.1016/j.jemermed.2009.02.003

TraumaReports1

EVALUATION AND MANAGEMENT OF MODERATE TO SEVERE PEDIATRICHEAD TRAUMA

Anand Swaminathan, MD, MPH,* Phil Levy, MD,†‡ and Eric Legome, MD§

*New York University (NYU)/Bellevue Emergency Medicine Residency, Department of Emergency Medicine, NYU Medical Center, NewYork, New York, †Department of Emergency Medicine, Detroit Receiving Hospital, Detroit, Michigan, ‡Emergency Medicine Residency,

Wayne State University School of Medicine, Detroit, Michigan, and §Department of Emergency Medicine, St. Vincent’s HospitalManhattan, New York, New York

Reprint Address: Eric Legome, MD, Department of Emergency Medicine, St. Vincent’s Hospital Manhattan, 103 West 12th Street, New

York, NY 10011

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Abstract—A case of pediatric head trauma is presentedith a detailed discussion of current concepts in evaluationnd treatment. Management of the moderate to severeead-injured child is reviewed, and best practices for emer-ency department treatment are discussed. Background:ediatric head trauma is a common and potentially devas-

ating injury. Thorough knowledge of the clinical evalua-ion and treatment will assist the emergency physician inroviding optimal care. Discussion: Using a case-based sce-ario, the initial management strategies along with ratio-ale evidence-based treatments are reviewed. Conclusions:omputed tomography scan is the diagnostic test of choice

or the moderate to severe head-injured pediatric patient.everal unique scales to describe and prognosticate theead injury are discussed, although currently, the Glasgowoma Scale is still the most commonly accepted one. Sim-

lar to the adult patient, avoidance of hypotension andypoxia are key to decreasing mortality. Etomidate anduccinylcholine remain the choice of medications for intu-ation. Hyperventilation should be avoided. © 2009lsevier Inc.

Keywords—pediatric head trauma; resuscitation; TBI;ediatric critical care

Trauma Reports of NYU/Bellevue Emergency Medicineesidency, New York, NY.

ECEIVED: 24 September 2008; FINAL SUBMISSION RECEIVE

CCEPTED: 5 February 2009

63

CASE PRESENTATION

35-day-old ex-premature 35-week boy was brought iny Emergency Medical Services (EMS) after a witnessedall out of a baby carrier down 15 carpeted steps. Thearents stated that the child continued breathing, but wastherwise unresponsive to voice or pain for 30 s, andhen began to cry inconsolably. They denied witnessingomiting or seizure-like activity after the fall. EMS se-ured the patient in his baby carrier and transported thehild to the Emergency Department (ED). En route, theatient was crying, with episodes of decreased respon-iveness. On ED arrival, vital signs revealed a bloodressure of 51/24 mm Hg, a heart rate of 171 beats/min,espiratory rate of 44 breaths/min, and an oxygen satu-ation of 100% on room air.

On primary survey, the airway appeared patent.reathing was normal and breath sounds were equalilaterally. The child was pink in color with strongrachial and femoral pulses bilaterally. He opened hisyes to painful stimuli but not spontaneously, and wouldove all four extremities equally without any specific

esponse to pain. The patient made no vocal response.he initial pediatric Glasgow Coma Scale (GCS) was 6.

Immediately upon arrival, intravenous access was es-ablished, the patient was placed on a monitor, and

January 2009;

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low-by oxygen was delivered. The patient’s neck waslso immobilized.

Secondary survey revealed a large hematoma over theeft frontoparietal region without any evidence of lacer-tion. The anterior fontanelle was open and flat and thereere no palpable skull fractures. Pupils were 5 mmilaterally and reactive to light. The chest, abdomen, andxtremity examinations were unremarkable. A bedsideAST (focused assessment with sonography in trauma)xamination revealed no evidence of free intra-peritonealuid or pericardial effusion.

After the secondary survey was completed, the patientad recurrent, intermittent apneic episodes lasting 5–6 sach. Bag-valve-mask ventilation was initiated and intu-ation was attempted. Intubation was complicated bymesis and desaturation, but eventually the airway wasecured. Because the blood pressure after intubation was5/23 mm Hg, a 60-cc bolus of normal saline was ad-inistered, with a resultant increase in blood pressure to

7/35 mm Hg.

BACKGROUND

oughly 650,000 children each year in the United Statesre evaluated in the ED for head trauma, 80% of whichre considered minor events. Despite this, head traumaemains the principal cause of trauma-related morbiditynd mortality in the pediatric population. The degree ofead trauma is defined by the presenting GCS, where acore of 14–15 is defined as mild (occasionally 13 isncluded in mild), 9–13 as moderate, and 3–8 as severe.lthough falls exist as the primary etiology of head

rauma in children � 2 years of age, abuse stands as theeading cause of severe cranial injury. The overall mor-ality rate of isolated severe pediatric head injury is–10%, which is significantly better than the 30–50%ortality rates in similarly injured adults (1). In addition,

0% of patients that present with GCS scores of 3 or 4ave good neurologic recovery and 95% of severe pedi-tric head trauma patients over the age of 5 years wereble to return to the appropriate grade level (1).

The pathophysiology of pediatric head injury, how-ver, differs substantially from that of adult head injury.pen cranial sutures result in increased susceptibility to

njury from blunt forces and delay the onset of herniations they allow for a greater amount of intracranial expan-ion. Pediatric brains are also less myelinated thandults, predisposing them to shearing forces (2,3). Theffects of hypoxia, hypotension, and intracranial hyper-ension on neurologic outcome are more profound inediatric head trauma patients, primarily due to the de-elopment of secondary brain injury. Secondary brain

njury is the delayed cellular damage and dysfunction, i

hich develops subsequent to the initial or primary insultnd is influenced by both intracranial and systemic fac-ors. As such, there is potential to decrease or amelioratets intensity, duration, and ultimate effect on outcomehrough early, aggressive, comprehensive patient care.able 1 comprises the major causes of secondary injury.

DISCUSSION OF INITIAL MANAGEMENT

n expedited assessment of airway and breathing isssential. Hypoxia is a leading cause of secondary neu-onal injury and must be promptly reversed. The pres-nce of hypoxia has been associated with a two- toourfold increase in poor outcomes, as defined by death,evere disability, or persistent vegetative state (4). Earlyirway management ensures oxygenation and decreaseshe risk of respiratory compromise due to secondaryerebral edema affecting the respiratory center. The de-ision to intubate the head-injured patient is a clinicalne, with mental status serving as the primary factor ofmportance. For adults, a GCS � 8 in the setting of headrauma is commonly considered an absolute indication tonitiate rapid establishment of a definitive airway; be-ause the GCS relies on verbal responses, such a rule cane difficult to apply to young children. A pediatric GCSith modified verbal response scores exists as a substi-

ute but is still of limited utility in infants (Table 2). Thenfant face scale (IFS) (Table 3) was developed to ad-ress this deficiency and serves as a useful adjunct in thevaluation of head-injured young patients (5). Despite itsotential, the IFS is not widely used to guide the man-gement of pediatric traumatic brain injury (TBI) be-ause its use has not been standardized in infants andhildren. In addition, unlike in adults, there is no widelyccepted IFS score that indicates the need for intubation.hus, most pediatric literature continues to base recom-endations on GCS scores. Because severe agitation can

nterfere with stabilization and patient management,any advocate early intubation for these patients as well.Rapid sequence intubation (RSI) with sedation and

aralysis is the preferred technique for airway manage-ent in patients with suspected TBI. Based on the belief

hat children have a more pronounced vagal response to

able 1. Major Causes of Secondary Brain Injury

ypoxia Hypotensionyperthermia Hyperglycemia/hypoglycemia

ntracranial hypertension Hypocapnia/hypercapnianemia Cerebral edemaasospasm Seizuresompression from mass effect

ntubation, pre-medication with atropine before administra-

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Evaluation and Management of Pediatric Head Trauma 65

ion of sedative and paralytic agents has been advocated forhe pediatric population (6–8). Recent literature, however,as demonstrated equivalence in the incidence of vagallyediated bradycardia during laryngoscopy and intubation

n pediatric patients who were pre-medicated with atro-ine vs. those that were not, regardless of the paralyticgent used (9,10). Although there is minimal downsideo the use of atropine before intubation, it does causeydriasis, which can last for hours. This effect removes

he clinician’s ability to diagnose brain herniation basedn pupillary response and may delay emergency decom-ressive measures. Intravenous lidocaine use has alsoeen advocated before initiation of RSI, largely based onhe theoretical ability of this medication to blunt theransient rise in intracranial pressure (ICP) that occursith laryngeal instrumentation. However, there is a lackf evidence supporting either reduction in ICP or im-rovement in neurological outcome with lidocaine useefore RSI (11). Because pretreatment strategies requireime to achieve desired effect, they may delay the inter-al to definitive airway control. Therefore, they shoulde utilized, if at all, only when airway compromise is notmminent.

Once a decision has been made to perform RSI,hoice of sedative agent is important. Medications suchs thiopental, propofol, and midazolam should be usedautiously due to their propensity to cause hypotensionnd thus lower cerebral perfusion pressure (12). Thedeal agent is one that does not compromise the patients’emodynamic parameters. The use of ketamine for in-uction has been discouraged due to the belief that itncreased ICP, cerebral oxygen consumption, and cere-ral metabolism, primarily via inhibitory effect on cate-

able 2. Pediatric Glasgow Coma Score (GCS)

Assessed Response Score

est eye responseSpontaneously 4To verbal stimulation or to touch 3To pain 2No response 1

est verbal responseSmiles, oriented to sounds, follows objects, interacts 5Cries but is consolable, inappropriate interactions 4Inconsistently consolable, moaning 3Inconsolable, agitated 2No vocal response 1otorNormal spontaneous movement 6Withdraws to touch 5Withdraws to pain 4Flexion abnormal 3Extension, either spontaneous or to painful stimuli 2Flaccid 1

holamine reuptake. However, more recent, although not

efinitive, studies argue against the detrimental effectsn ICP (13–15). In addition, ketamine maintains meanrterial pressure, thus avoiding hypotension during RSI.tomidate is a rapid-acting, short-duration sedative withinimal hemodynamic effects. Etomidate is also thought

o exert neuroprotective effects through a decrease inCP and a reduction in the metabolic rate and oxygenonsumption of the brain, making it an ideal agent forse in TBI (16,17).

Succinylcholine has been used as the paralytic agent ofhoice for RSI in both adults and children. The onset ofuccinycholine is approximately 45 s, and the durationf action is 3–5 min. Because it is a depolarizing para-ytic agent, succinylcholine may elevate ICP transiently,ut there is no clinical evidence of an associated increasen morbidity or mortality related to its use (18,19). Non-epolarizing paralytic agents such as rocuronium may beubstituted to avoid the potential for increased ICP, buthey have a delayed onset of action and prolonged pa-alysis in comparison to succinycholine. Higher doses ofocuronium (1.2 mg/kg) have been shown to yield com-arable onset times to succinylcholine, but a recentochrane review concluded that succinylcholine was

uperior due to its shorter duration of action (20,21).retreatment with a defasciculating dose (1/10th of thetandard dose) of a non-depolarizing agent before admin-stration of succinycholine may diminish the develop-ent of fasciculations (which are thought to be respon-

able 3. Infant Face Scale (IFS)

Assessed Response Score

ye openingSpontaneously 4To verbal stimulation or to touch 3To pain 2No response 1

erbal/facial responseCries (grimaces with crying sounds or tears)

spontaneously, with handling, or to minor pain;alternating with periods of quiet wakefulnesswhen not asleep

5

Cries (grimaces with crying sounds or tears)spontaneously, with handling, or to minor pain;alternating with sleep only (no quietwakefulness maintained)

4

Cries to deep pain only 3Grimaces only to pain (facial movement without

sounds or tears)2

No facial expression to pain 1otorSpontaneous normal movements 5Spontaneous normal movements reduced in

frequency or excursion; hypoactive5

Non-specific movement to deep pain only 4Abnormal rhythmic spontaneous movements;

seizure-like activity3

Extension, either spontaneous or to painful stimuli 2

Flaccid 1

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ible for the increase in ICP) but to date, no studies haveemonstrated the efficacy of this and it is not routinelyecommended (22).

In the past, aggressive hyperventilation was com-only performed in an effort to reduce ICP in those withBI (23). This was based on the assumption that brainyperemia was common after TBI and that hyperventila-ion would restore blood pressure autoregulation throughnduced hypocapnia, thereby improving cerebral metabo-ism and selectively increasing perfusion to ischemic areas.yperventilation is known, however, to cause cerebralasoconstriction with an associated decrease in cerebrallood flow. Although early studies reported a clinicalenefit from hyperventilation, more recent data show anssociation with worsened neurological outcomes, thats, greater likelihood of moderate to severe disability24–26). This is thought to be related to a combination ofyperventilation-induced ischemia in both injured andntact parts of the brain secondary to decreasing cerebrallood flow and a depletion of bicarbonate in the brainith resultant impairment in buffering capacity. As such,

urrent recommendations are for ventilation to be titratedo eucapnea, with reservation of hyperventilation solelyor TBI patients who demonstrate signs of impendingerebral herniation.

Children with moderate to severe head injury are alsot risk for associated cervical spine injuries. Duringntubation, therefore, in-line cervical spine immobiliza-ion must be maintained to prevent further injury. Therevalence of cervical spine injury in adult severe bluntead injury is estimated to be 6–8% (27,28). Pediatricpinal cord injuries are much less common than in adults,ccounting for only 0.3–10% of all spinal cord injuries29). Sixty to eighty percent of all spinal cord injuries inatients � 8 years of age occur in the cervical spine dueo the relatively larger head and underdeveloped neckuscles (only 30–40% of spinal cord injuries in adults

re in the cervical spine) (30).Once the airway has been secured and ventilation

stablished, the patient’s circulatory status must be ad-ressed. Hypotension is the most influential secondaryrain insult determining short-term mortality, with ahreefold increase (61% vs. 22%) after the occurrence of

single episode (31,32). Although hypotension is de-ned in the pediatric literature as a systolic blood pres-ure measurement below the fifth percentile of normalor age, Vavilala et al. demonstrated an increase in mor-ality for TBI patients when systolic blood pressure dropselow the 75th percentile (33). Although isolated headrauma can cause hypotension in children, alternativeources such as blood loss from other injuries should beought. Prompt fluid resuscitation with normal salinehould be initiated immediately to avoid hypotension.

lthough some research has found that children suffer-

tr

ng TBI with elevated systolic blood pressures hadigher survival rates, there is currently no role for induc-ng supranormal blood pressure (34).

FURTHER MANAGEMENT IN THEEMERGENCY DEPARTMENT

efore diagnostic imaging, the patient had a generalizedonic-clonic seizure. Phenobarbital was administered,ith cessation of seizure activity. The patient was then

ransported to Radiology, where computed tomographyCT) scanning of the head, cervical spine, chest, abdo-en, and pelvis were obtained. Non-contrast head CT

NCHCT) revealed multiple intracranial injuries, includ-ng left anterior and posterior subgaleal hematomas, ainimally displaced left parietal bone fracture, left epi-

ural vs. subdural hematoma, right frontal subdural he-atoma, multiple areas of subarachnoid hemorrhage,

ight temporal horn hemorrhagic contusion, and a leftateral ventricle interventricular hemorrhage, but no ev-dence of midline shift or mass effect (Figure 1). Cervicalpine CT scan demonstrated no fractures, and CT scansf the chest, abdomen, and pelvis showed no injuries. Oneturn to the ED, the patient was loaded with intravenoushenytoin for further seizure prophylaxis.

OTHER ACUTE INTERVENTIONS

ediatric critical care consensus statements recommendggressive ICP-directed therapy in all children with se-

igure 1. Non-contrast head computed tomography scan of

he patient. Thick arrow: subarachnoid hemorrhage; thin ar-ow: subdural hemorrhage; triangle: intraventricular blood.

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Evaluation and Management of Pediatric Head Trauma 67

ere TBI and a GCS score � 8 (35). The literatureupporting these recommendations is comprised of aumber of small, single-center, observational and retro-pective studies. No randomized controlled trial has beenerformed in any age group evaluating the effect of ICPonitoring on long-term neurologic outcomes. Intracra-

ial hypertension is a major predictor of poor neurologicutcome and increased mortality but can be controlledith medical interventions (hyperosmolar and hyperven-

ilation therapy) as well as surgical interventions (cere-ral spinal fluid drainage and decompressive craniot-my). A discussion of these interventions is beyond thecope of this review, but it is important to appropriatelydentify those patients, using historical and clinical fac-ors combined with imaging, who may require earlyeurosurgical intervention and aggressive ongoing man-gement. Clinical accuracy for this, however, is limited.pen fontanels and sutures do not prevent the develop-ent of increased ICP or diminish the utility of ICPonitoring (36). Studies demonstrate that up to 86% of

hildren with an initial GCS � 8 had ICP measurements20 mm Hg (37). In addition, 53–63% of patients with

evere TBI in combination with abnormal NCHCT hadlevated ICP (38). A normal admission NCHCT does notule out increased ICP (39).

Non-surgical management of pediatric patients withonfirmed or suspected increases in ICP can be challeng-ng. Prophylactic use of hyperosmolar therapy (mannitolr hypertonic saline) in children with severe TBI is notdvocated. Current recommendations are to use thesegents only in conjunction with an ICP monitor andocumented elevation in ICP (40,41). However, manni-ol may be given empirically for signs and symptoms oferniation or impending herniation. This includes acuteecline in mental status and unilateral dilatated and un-esponsive pupil. Prophylactic anti-seizure medication isppropriate to initiate, and use of these agents should beontinued for 7 days in all patients with moderate toevere head trauma defined as an initial GCS � 8 (42).o one agent has been clearly proven superior. Up

o 40% of these patients will experience early post-raumatic seizures (43). The risk of seizure developmentncreases threefold in children under the age of 2 yearsvs. those older than the age of 12) (44). Seizures canause secondary brain injury by a number of differentechanisms, including hypoxia, hypercarbia, and in-

reased cerebral metabolic demand, and will cause fur-her increases in ICP. Multiple studies have demon-trated reduction in the incidence of early post-traumaticeizures with the use of anti-seizure medications, buthere are no well-designed studies to suggest a preferredr superior agent (42,45). It is important to remember

owever, that early seizure prophylaxis does not affect

he risk of developing late post-traumatic (� 7 days aftervent) seizures (46).

DISCUSSION

he management of pediatric head trauma in the EDocuses on rapid stabilization, diagnosis, and attempts toeduce the development of secondary brain injury. Ap-ropriate interventions can have a significant effect oneurologic outcome. Hypoxia and hypotension must bevoided or rapidly corrected due to the association ofach with extremely poor outcomes. Early definitiveirway control should be considered in all patients botho avoid hypoxia and facilitate further management. Hy-erventilation should be avoided unless signs of hernia-ion are present, as it has been shown to increase cerebralschemia. Early seizure prophylaxis should be initiated inll patients with severe TBI. Finally, because many ofhe necessary therapeutic modalities rely on invasiveonitoring, close cooperation between the emergency

hysician and neurosurgeon is necessary.

CONCLUSION

he patient was evaluated by the neurosurgical servicend it was determined that acute invasive surgical inter-ention was not indicated, as there was not an easilydentifiable lesion causing mass effect that would bemenable to operative removal. The patient was admittedo the Pediatric Intensive Care Unit and repeat NCHCTemonstrated no change in the injury patterns previouslyescribed. On hospital day 3, the patient was success-ully extubated and enteral feeds were started. RepeatCHCT on hospital day 6 showed evidence of resolving

ubdural and intraventricular hemorrhage. The patientas discharged home on hospital day 7 on a phenobar-ital taper. At the time, the patient showed appropriateeurological development for his age. Due to the pa-ient’s young age, the potential for long-term neurologicequelae remained uncertain upon discharge.

REFERENCES

1. Mayer TA, Walker ML. Pediatric head injury: the critical role ofthe emergency physician. Ann Emerg Med 1985;14:1178–84.

2. King DR. Trauma in infancy and childhood: initial evaluation andmanagement. Pediatr Clin North Am 1985;32:1299–310.

3. Ghajar J, Hariri RJ. Management of pediatric head injury. PediatrClin North Am 1992;39:1093–125.

4. Ong L, Selladurai BM, Dhillon MK, et al. The prognostic value ofthe Glasgow Coma Scale, hypoxia and computed tomography in

outcome prediction of pediatric head injury. Pediatr Neurosurg1996;24:285–91.

1

1

1

1

1

1

1

1

1

1

2

2

2

2

2

2

2

2

2

2

3

3

3

3

3

3

3

3

3

3

4

4

4

4

4

4

4

68 A. Swaminathan et al.

5. Berger RP, Adelson PD. Evaluation and management of pediatrichead trauma in the emergency department: current concepts andstate-of-the-art research. Clin Pediatr Emerg Med 2005;6:8–15.

6. Yamamoto LG, Yim GK, Britten AG. Rapid sequence anesthesiainduction for emergency intubation. Pediatr Emerg Care 1990;6:200–13.

7. Tobias JD. Airway management for pediatric emergencies. PediatrAnn 1996;25:317–28.

8. McAllister JD, Gnauck KA. Rapid sequence intubation of thepediatric patient. Pediatr Clin North Am 1999;46:1249–84.

9. Fastle RK, Roback MG. Pediatric rapid sequence intubation: inci-dence of re-flex bradycardia and effects of pretreatment withatropine. Pediatr Emerg Care 2004;20:651–5.

0. Bean A, Jones J. Atropine: re-evaluating its use during paediatricRSI. Emerg Med J 2007;24:361–2.

1. Robinson N, Clancy M. In patients with head injury undergoingrapid sequence intubation, does pretreatment with intravenouslignocaine/lidocaine lead to an improved neurological outcome? Areview of the literature. Emerg Med J 2001;18:453–7.

2. Zelicof-Paul A, Smith-Lockridge A, Schnadower D, et al. Contro-versies in rapid sequence intubation in children. Curr Opin Pediatr2005;17:355–62.

3. Bourgoin A, Albanese J, Wereszczynski N, et al. Safety of sedationwith ketamine in severe head injury patients: comparison withsufentanil. Crit Care Med 2003;31:711–7.

4. Bourgoin A, Albanese J, Leone M, Sampol-Manos E, Viiand X,Martin C. Effects of sufentanil or ketamine administered in target-controlled infusion on the cerebral hemodynamics of severelybrain-inured patients. Crit Care Med 2005;33:1109–13.

5. Himmelesher S, Durieux ME. Revising a dogma: ketamine forpatients with neurological injury? Anesth Analg 2005;101:524–34.

6. Bergen JM, Smith DC. A review of etomidate for rapid sequenceintubation in the emergency department. J Emerg Med 1997;15:221–30.

7. Modica PA, Tempelhoff R. Intracranial pressure during inductionof anaesthesia and tracheal intubation with etomidate-induced EEGburst suppression. Can J Anesth 1992;39:36–41.

8. Brown MM, Parr MJ, Manara AR. The effect of suxamethoniumon intracranial pressure and cerebral perfusion in patients withsevere head injuries following blunt trauma. Eur J Anaesth 1996;13:474–77.

9. Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine doesnot change intracranial pressure, cerebral blood flow velocity, orthe electroencephalogram in patients with neurologic injury.Anesth Analg 1994;78:469–73.

0. Verma RK, Goordayal R, Jaiswal S, Sinha GK. A comparativestudy of the intubating conditions and cardiovascular effects fol-lowing succinylcholine and rocuronium in adult elective surgicalpatients. Internet J Anesthesiol 2007;14(1).

1. Perry JJ, Lee JS, Sillberg VAH, Wells GA. Rocuronium versussuccinylcholine for rapid sequence induction intubation. CochraneDatabase Syst Rev 2007;(3):CD002788.

2. Clancy M, Halford S, Walls R, Murphy M. In patients with headinjuries who undergo rapid sequence intubation using succinylcho-line, does pretreatment with a competitive neuromuscular blockingagent improve outcome? A literature review. Emerg Med J 2001;18:373–5.

3. Bruce D, Raphaely R, Goldberg A, et al. Pathophysiology, treat-ment and outcome following severe head injury in children. ChildsBrain 1979;5:174–9.

4. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects ofprolonged hyperventilation in patients with severe head injury: arandomized clinical trial. J Neurosurg 1991;75:731–9.

5. Skippen P, Seear M, Poskitt K, et al. Effect of hyperventilation onregional cerebral blood flow in head-injured children. Crit CareMed 1997;25:1402–9.

6. Stringer WA, Hasso AN, Thompson JR, Hinshaw DB, Jordan KG.Hyperventilation-induced cerebral ischemia in patients with acutebrain lesions: demonstration by Xenon-enhanced CT. AJNR Am J

Neuroradiol 1993;14:475–84.

7. Hills MW, Deane SA. Head injury and facial injury: is there anincreased risk of cervical spine injury? J Trauma 1993;34:549–54.

8. Michael DB, Guyot DR, Darmody WR. Coincidence of head andcervical spine injury. J Neurotrauma 1989;6:177–89.

9. Dias MS. Traumatic brain and spinal cord injury. Pediatr ClinNorth Am 2004;51:271–303.

0. Cirak B, Ziegfeld S, Knight VM, Chang D, Avellino AM, PaidasCN. Spinal injuries in children. J Pediatr Surg 2004;39:607–12.

1. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for theacute medical management of severe traumatic brain injury ininfants, children, and adolescents. Chapter 4. Resuscitation ofblood pressure and oxygenation and pre-hospital brain-specifictherapies for the severe pediatric traumatic brain injury patient.Pediatr Crit Care Med 2003;S12–8.

2. Pigula FA, Wald SL, Shackford SR, et al. The effect of hypoten-sion and hypoxia on children with severe head injuries. J PediatrSurg 1993;28:310–4.

3. Vavilala MS, Bowen A, Lam AM, et al. Blood pressure andoutcome after severe pediatric traumatic brain injury. J Trauma2003;55:1039–44.

4. White JR, Farukhi Z, Bull C, et al. Predictors of outcome inseverely head-injured children. Crit Care Med 2001;29:534–50.

5. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for theacute medical management of severe traumatic brain injury ininfants, children and adolescents. Chapter 5. Indications forintracranial pressure monitoring in pediatric patients with se-vere traumatic brain injury. Pediatr Crit Care Med 2003;4(3Suppl):S19 –24.

6. Cho DY, Wang YC, Chi CS. Decompressive craniotomy for acuteshaken/impact syndrome. Pediatr Neurosurg 1995;23:192–8.

7. Shapiro K, Marmarou A. Clinical applications of the pressure-volume index in treatment of pediatric head injuries. J Neurosurg1982;56:819–25.

8. Narayan RK, Kishore PR, Becker DP, et al. Intracranial pressure:to monitor or not to monitor? A review of our experience withsevere head injury. J Neurosurg 1982;56:650–9.

9. O’Sullivan MG, Statham PF, Jones PA, et al. Role of intracranialpressure monitoring in severely head injured patients without signsof intracranial hypertension on initial CT. J Neurosurg 1994;80:46–50.

0. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for theacute medical management of severe traumatic brain injury ininfants, children and adolescents. Chapter 11. Use of hyperosmolartherapy in the management of severe pediatric traumatic braininjury. Pediatr Crit Care Med 2003;4(3 Suppl):S40–4.

1. Qureshi AI, Geocadin RG, Suarez JI, Ulatowski JA. Long-termoutcome after medical reversal of transtentorial herniation in pa-tients with supratentorial mass lesions. Crit Care Med 2000;28:1556–64.

2. Lewis RJ, Yee L, Inkelis SH, et al. Clinical predictors of post-traumatic seizures in children with head trauma. Ann Emerg Med1993;22:1114–8.

3. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acutemedical management of severe traumatic brain injury in infants,children and adolescents. Chapter 12. Use of hyperventilation in theacute management of severe pediatric traumatic brain injury. PediatrCrit Care Med 2003;4(3 Suppl):S45–8.

4. Ratan SK, Kulshreshtha R, Pandey RM. Predictors of posttrau-matic convulsions in head-injured children. Pediatr Neurosurg1999;30:127–31.

5. Tilford JM, Simpson PM, Yeh TS, et al. Variation in therapy andoutcome for pediatric head trauma patients. Crit Care Med 2001;29:1056–61.

6. Adelson PD, Bratton SL, Carney NA, et al. Guidelines for theacute medical management of severe traumatic brain injury ininfants, children and adolescents. Chapter 19. The role of anti-seizure prophylaxis following severe pediatric traumatic brain in-

jury. Pediatr Crit Care Med 2003;4(3 Suppl):S72–5.