Trauma Pediatric - part 6 pot

Because pediatric patients are not simplysmall adults, therapy should be based on scientific evidence that a particular type oftreatment will actually improve a child’s outcome from traum

27 Sessler DI Perioperative thermoregulation and heat balance Ann New York Acad Sci1997; 813:757–777.

28 Handrigan MT, Wright RO, Becker BM, Linakis JG, Jay GD Factors and methodology

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29 Bernardo LM, Henker R, Bove M, Sereika S The effect of administered crystalloid fluidtemperature on aural temperature of moderately and severely injured children J EmergNursing Online 1997; 23(2)

30 Sieunarine K, White G Full thickness burn and venous thrombosis following nous infusion of microwave heated crystalloid fluids Burns 1996; 22(7):568–569

intrave-31 Neville H, Lally K, Cox C Emergent abdominal decompression with patch plasty in the pediatric patient J Pediat Surg 2000; 35(5):705–708

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S, Tetik Analysis of 33 pediatric trauma victims in the 1999 Marmara earthquake, inBritish Association of Pediatric Surgeons 17th Annual International Congress, Sorrento,Italy, 2000

35 Partrick DA, Bensard DD, Moore EE, Partington MD, Karrer FM Driveway crushinjuries in young children: a highly lethal, devastating, and potentially preventable event

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43 Reznik VM, Griswold WR, Peterson BM, Rodarte A, Ferris ME, Mendoza SA neal dialysis for acute renal failure in children Pediatr Nephrol 1991; 5:715–717

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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 pediatricpopulation Despite this, data from well-designed clinical studies, which could beused to guide the management of children with severe traumatic brain injury, arescarce Most of the randomized controlled trials designed to evaluate head injuryhave excluded pediatric patients Because of the paucity of proven therapies inpediatric head injury, management strategies for severely head-injured children aregenerally extrapolated from adult studies Because pediatric patients are not simplysmall adults, therapy should be based on scientific evidence that a particular type oftreatment will actually improve a child’s outcome from traumatic brain injury.Many of the therapies that are routinely employed in the treatment of adultswith 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 onexpert opinion and practice experience This has resulted in tremendous variations inthe treatment and outcomes of head-injured patients, with mortality rates rangingfrom 25% to 60% In an attempt to standardize the care of patients with severe headinjury and ultimately improve outcome, the American Association of NeurologicalSurgeons and the Brain Trauma Foundation performed a thorough review of theexisting head injury literature and developed evidence-based standards, guidelines,and treatment options for managing adult patients with severe head injury (1) Theseguidelines 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 Thefollowing topics, which were deemed to have an impact on the outcome of patientswith 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

211

For most of the clinical practice parameters addressed in this publication, therewere 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 thetreatment of severe head 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 latepost-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 common in pediatrictrauma than in adult trauma, no specific recommendations were made in the adultguidelines regarding the treatment of traumatic brain injury in pediatric patients Asubsequent meticulous analysis of this publication for relevance to the manage-ment of severe pediatric head injury revealed even fewer recommendations forstandards of care (2) In an attempt to standardize and improve treatment practiceand patient outcome in pediatric patients with severe head injury, a multidisciplin-ary team of clinicians and researchers recently reviewed all the available data onthis topic and subsequently published evidence-based practice standards, guide-lines, and treatment options for the acute medical management of pediatricpatients with severe traumatic brain injury (3) In the pediatric guidelines as inthe adult guidelines practice standards refer to accepted principles of patient man-agement that reflect a high degree of clinical certainty (i.e., they are basedpredominantly on class I data, derived from randomized controlled trials, as well

as on some strong class II data, derived mainly from prospective and some 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 onclasses II and III data, derived from retrospective studies such as clinical series,case reports, expert opinions, and databases or registries) Finally, treatmentoptions refer to management strategies for which the clinical certainty is unclear(i.e., they are based solely on class III data or represent the consensus of experts

retro-in areas where studies documentretro-ing more definitive levels of certaretro-inty are not able or are not possible) Besides elucidating scientific evidence that supports var-ious treatment strategies and the rigor of the evidence, this analysis on thetreatment of severe pediatric head injury revealed that pediatric head injury isunder investigated and that many questions remain unanswered, especially at theclass I level, regarding the optimal medical and surgical management of severetraumatic brain injury in the pediatric population (3) Thus, large, well-designed,prospective, randomized, controlled multicenter trials are still needed to investigateadditional treatment modalities and provide standards of care for the management

avail-of severe pediatric head injury

The present chapter discusses current therapeutic options for the management

of severe head injury in pediatric patients Aspects of care covered in this chapterinclude both prehospital and intensive management of pediatric patients with severehead 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 whoare 17 years of age or younger; severe head injury is defined using the Glasgow Coma

Scale with a score equal to or less than eight; and traumatic brain injury includesboth accidental and non-accidental causes (4).

PATHOPHYSIOLOGY OF HEAD INJURY

Before proceeding with a discussion on evidence-based management strategies forthe 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 ofinjury—primary and secondary Primary injury arises at the time of the traumaticevent and generates the initial damage that occurs at the moment of impact, includ-ing structural damage to neurons, supporting tissues, and blood vessels Examples ofprimary injury include skull fracture, epidural and subdural hematomas, intrapar-enchymal hemorrhage, cortical contusions, diffuse axonal injury, and brain steminjury In contrast, secondary injury is an evolving process that develops duringthe hours and days that follow the initial trauma and produces additional progres-sive cellular damage and dysfunction resulting 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 primaryinjury, 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, traumaticischemia and/or infarction, secondary hemorrhage, hypotension, and hypoxia Thus,only part of the damage to the brain that occurs during head trauma takes place atthe 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 maximizethe potential for recovery Successful management of severe pediatric head injuryrequires complete and rapid physiologic resuscitation, prevention of hypotensionand hypoxia, treatment of elevated ICP, and maintenance of cerebral perfusion tofacilitate adequate delivery of oxygen and metabolic substrates to the brain.The developing/maturing brain of a child undergoes changes that affect itssusceptibility to both primary and secondary injury For example, children have lesscerebrospinal fluid volume, which results in less buffering capacity for changes inintracranial tissue volume and places them at risk for earlier decompensation andsecondary ischemia after traumatic brain injury Open fontanels and expandablecalvarial sutures do not add buffering capacity and, therefore, are not protective

in head-injured infants Because of these and many other differences that existbetween pediatric and adult patients, the treatment of head injury in the pediatricpopulation should not be based on generalizations from studies in adults but rathershould rely on scientific evidence derived from studies on pediatric patients Theremainder of this chapter focuses on evidence-based management strategies for thetreatment of severe pediatric head injury

EVIDENCE-BASED TREATMENT STRATEGIES—

PRE-HOSPITAL CARE

Speed of access to definitive care and timing of the intervention relative to the initialinsult 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

decreased mortality rate in severely head-injured pediatric patients treated inpediatric trauma centers (5–8) However, as pointed out in the recently establishedpediatric 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 IVrural hospitals then transferred to a higher level of care, had a significantly increasedmortality 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 centerand then transferred to a pediatric trauma center Based on this, the followingrecommendations were made in the pediatric guidelines (3):

1 Pediatric patients with severe traumatic brain injury should be transporteddirectly to and treated in a pediatric trauma center if available (guideline)

or to an adult trauma center staffed with qualified, pediatric-trainedcaregivers and equipment necessary for treating pediatric patients if nopediatric trauma center is available (option)

2 Although the literature provides strong evidence to support a role fortrauma systems and pediatric trauma centers in the increased survival ofpediatric patients with severe head injury, their role on the eventual func-tional outcome of pediatric patients with severe head injury remainsunclear

Airway Management

Hypoxemia, which commonly occurs during the prehospital care of severely injured children is associated with poorer functional outcomes in pediatric patientswith traumatic brain injury (10–13) Despite this, evidence suggesting that aggressiveprehospital airway management (i.e., endotracheal intubation over bag-valve-maskventilation) improves outcome for children with traumatic brain injury is lacking(14) The pediatric guidelines make two recommendations regarding the prehospitalmanagement of airway in severely head-injured pediatric patients (3):

head-1 Avoid hypoxia if possible or correct it immediately by administering lemental oxygen (guideline),

supp-2 Perform endotracheal intubation in the prehospital setting guided by tidal CO2detectors and only by scene-critical care providers who are speci-fically trained to intubate pediatric patients (option)

end-If qualified caregivers are unavailable, then bag-valve-mask ventilation should

be carried out until the patient reaches a trauma center staffed with the appropriatelytrained personnel in order to prevent life-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 ofimpact, progressive cellular damage and dysfunction frequently occur in the ensuinghours and days as a consequence of degenerative biochemical processes initiatedboth by the primary injury and by additional systemic insults such as hypotensionand hypoxia Because of the exquisite sensitivity of the injured brain to secondarysystemic and local intracranial insults, they must be avoided in order to minimizethe progression of brain injury and maximize the potential for recovery (15–21)

Hypotension and hypoxia, which commonly occur in pediatric patients withsevere traumatic brain injury, have the greatest negative impact on outcome, includ-ing increased morbidity and mortality (12,17,22–27) For example, in a prospectivestudy 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 ofhypoxia and hypotension on mortality from severe traumatic brain injury in childrenhypotension on admission was associated with a mortality rate of 61%, whichincreased to 85% when both hypotension and hypoxia were present, compared withonly 22% when patients were normotensive on admission (17) Finally, in a prospec-tive analysis of severe traumatic brain injury in 6908 adults and 1906 childrenyounger than 15 years of age at 41 trauma centers, hypotension was associated withsignificantly 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 fifthpercentile 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’sage in years by two, and then by adding this number to 70 mmHg (28) Becausepediatric patients can maintain their blood pressure in the face of significant volumedepletion and clinical signs of shock, it is imperative that the pediatric traumaticbrain injury patient be monitored closely for signs of decreased perfusion, includingtachycardia, urine output less than 1 mL/kg/hr, or capillary filling time greater thantwo seconds Patients who exhibit such signs, even in the face of a normal bloodpressure, undergo adequate resuscitation with intravenous fluids In addition, hypo-tensive patients or those showing signs of decreased perfusion should undergo athorough evaluation for extracranial sources of hypotension, including internalbleeding or spinal cord injury, and the source(s) should be corrected as rapidly aspossible Finally, there is no role for fluid restriction in the management of severelyhead-injured pediatric patients demonstrating clinical signs of shock (29)

Hypoxia in children is defined as PaO2 <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 sodes of apnea, or measured hypercarbia Hypoxia and hypoventilation commonlyoccur 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 ventilationwith 100% oxygen as needed in the resuscitation phase of care to avoid hypoxia andhypercarbia Moreover, it is essential to perform continuous monitoring of oxygena-tion and ventilation to avoid hypoxia and hypercarbia or to detect and correct them

epi-as rapidly epi-as possible to age-appropriate parameters

As with all other critically injured pediatric patients, the prehospital ment (i.e., in the field and during transport) of pediatric patients with severetraumatic brain injury is of paramount importance and must be optimized in orderoptimize outcome The goal of such management is to prevent secondary braininjury by obtaining early airway control and restoring oxygenation, ventilation,circulating blood volume, and blood pressure (i.e., the ABCs of resuscitation) Based

manage-on previous studies (12,17,22–27), the following recommendatimanage-ons were made in thepediatric guidelines (3) Treatment guidelines included recognizing and correctinghypotension as rapidly as possible with intravenous fluids and evaluating and treat-ing all associated extracranial injuries Treatment options included:

1 obtaining airway control in children with a Glasgow Coma Score 8 or inthe face of hypoventilation,

2 using assisted ventilation 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 usingpulse oximetry and end-tidal CO2monitoring and/or serial arterial bloodgas 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 rangefor age

In addition, although there are no pediatric studies to date that evaluate theeffect of brain-directed therapies in the prehospital setting, such as the use of seda-tion, analgesia, neuromuscular blockade, mannitol, hypertonic saline, or hyperven-tilation, on the outcome from severe pediatric traumatic brain injury, the pediatricguidelines made the following recommendations regarding the use of these thera-pies (3) Specifically, they recommended as a treatment option the prehospital use ofsedation, analgesia, and neuromuscular blockade to optimize transport of the pedia-tric patient with traumatic brain injury However, they recommended against theprophylactic use of mannitol and hyperventilation (i.e., 25 breaths per minute in achild and 30 breaths per minute in an infant) in pediatric patients with traumaticbrain injury in the prehospital setting except in euvolemic, normotensive patientsexhibiting definite signs of cerebral herniation, or acute neurologic deterioration.The prehospital prophylactic use of brain-directed therapies, such as mannitol andhypertension, 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 hypotensionand hypoxia are potentially avoidable secondary insults that significantly increasethe morbidity and mortality of severe pediatric traumatic brain injury patients,evidence suggesting that outcome from severe head injury is improved by preventinghypotension and hypoxia in the prehospital setting is lacking (3) Further studies areneeded in pediatric patients with severe head injury to assess the role of prehospitalhypotension and hypoxia on functional outcome, to ascertain treatment thresholdsfor hypotension and hypoxia, to evaluate the potential beneficial role of hyperten-sion, and to assess prehospital management protocols, including brain-directedtherapies, in order to optimize prehospital management and subsequent functionaloutcome of pediatric patients with severe head injury

EVIDENCE-BASED TREATMENT STRATEGIES—

INTENSIVE MANAGEMENT

The use of intensive management protocols has significantly reduced mortality andmorbidity in pediatric patients with severe head injury Such protocols include earlyintubation and rapid transport to an appropriate trauma care facility; prompt intra-venous fluid resuscitation; CT scanning; surgical evacuation of intracranial masslesions; and meticulous management in an intensive care unit setting, with continuousmonitoring of physiologic parameters Routine monitoring of pediatric patients withsevere head injury includes continuous invasive arterial blood pressure monitoring,

pulse oximetry, and monitoring of ICP, central venous pressure, temperature, end-tidalcarbon dioxide, and urine output The primary goal of intensive management of severepediatric head injury is to improve mortality rates and functional recovery by prevent-ing secondary injury to the brain caused by systemic hypotension, hypoxia, elevatedICP, and/or reduced cerebral perfusion pressure (CPP) To avoid secondary braininjury, normal, age-appropriate physiologic parameters must be maintained or promptintervention must occur when deviations in these parameters arise.

The CPP, defined as the mean arterial blood pressure (MAP) minus ICP, is thephysiologic variable that represents the pressure gradient driving cerebral blood flowand metabolite/oxygen delivery and, therefore, is related to cerebral ischemia Theharmful consequences of elevated ICP stem from its effect on regional and globalcerebral blood flow Pediatric patients with severe traumatic brain injury, especiallythose with subdural hematomas, large multifocal contusions, hypoxic injury, and/orgunshot wounds to the head, frequently develop significant brain swelling and/ordiffuse cerebral edema, which, 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 poorfunctional outcome, pediatric patients with severe head injury require aggressivemonitoring in the pediatric intensive care unit, including ICP monitoring, to enablerapid detection and correction of neurologic deterioration through medical and/orsurgical 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 matic brain injury, ICP monitoring and the medical and/or surgical treatment ofintracranial hypertension are mainstays in the management of severe pediatric headinjury and have become widely accepted practice Maintenance of physiologic ICP isnecessary to ensure adequate cerebral perfusion, which, in turn, is required for thedelivery of oxygen and metabolic substrates to neurons and supporting cells In addi-tion, physiologic ICP must be maintained to prevent cerebral herniations (caused bythe mechanical displacement of brain, cerebrospinal fluid, and blood vessels fromone cranial compartment to another) and subsequent cerebral infarction

trau-Several class III studies provide evidence to support an association betweenintracranial hypertension and poor neurologic outcome (22,30–32) Moreover, otherclass III studies provide strong evidence that accurate continuous monitoring of ICPwith effective treatment of elevated ICP in severely head-injured pediatric patientsresults in improved functional outcomes (33–36) Therefore, in pediatric patientswith severe head injury (i.e., GCS score  8 including infants), an ICP monitorshould 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, cisternaleffacement, midline shift, and/or multiple contusions on the admitting head CTscan In addition, the pediatric guidelines recommend at the option level that anICP 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 extracranial injuries (3).The goal of ICP management is to reduce the ICP enough to ensure anadequate 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

severe head injury, no absolute treatment thresholds have been established (3) In thepast, practitioners have used 15, 20, or 25 mmHg as the arbitrary upper limit,beyond which treatment is initiated All available evidence related to ICP thresholdscomes from class III studies (e.g., see Refs 31,34), which suggest that the pathologi-cal effects of elevated ICP are related both to the absolute peak of ICP as well as tothe length of time the ICP remains elevated Based on the results of these and othersimilar class III studies, the pathological ICP level for which treatment should beinitiated is 20 mmHg Also, as suggested in the pediatric guidelines interpretationand treatment of ICP, regardless of the threshold chosen, should be validated by fre-quent clinical examination, cranial imaging, and monitoring of physiologic variables,such as CPP and MAP (3) Finally, to ensure the best possible outcome related toICP management, one must pay strict attention to detail, repeatedly assessingchanges in ICP and ongoing responses to therapy.

Accurate and reliable methods for monitoring ICP in pediatric patients withsevere head injury include intraparenchymal fiberoptic catheter tip pressure transdu-cer devices (e.g., Camino fiberoptic ICP monitor; Camino Laboratories, San Diego,California; Ref 37), a ventricular catheter connected to an external strain gauge,and external strain gauge transducers According to the adult guidelines a ventricu-lar catheter connected to an external strain gauge transducer is the recommendedmethod for ICP monitoring in adult patients with severe head injury (1) Althoughthis method has the added therapeutic benefit of reducing elevated ICP with cere-brospinal fluid (CSF) drainage, continuous monitoring of ICP cannot be achievedwith this method, since ICP cannot be measured while CSF is draining To achieveaccurate, reliable and continuous monitoring of ICP concomitant with therapeuticcerebrospinal fluid (CSF) drainage, one should place both an intraparenchymalcatheter tip pressure transducer device for continuous monitoring of ICP and a ven-triculostomy catheter for CSF drainage In addition to enabling ICP monitoring andtherapeutic CSF drainage at the same time, this technique also enables periodic mea-suring of ICP by the ventriculostomy catheter, which can then be compared to theICP measured by the intraparenchymal catheter tip pressure transducer device toevaluate for measurement differences and drift Moreover, in pediatric patients withsevere head injury, fiberoptic ICP monitoring is safe and effective with a lowmechanical failure rate, low risk of infection despite prolonged use of fiberopticmonitors, and low incidence of complications (e.g., hemorrhage) associated withplacement of these monitors (38)

Cerebral Perfusion Pressure

There is increasing evidence that cerebral blood flow is reduced as a consequence ofvasospasm following traumatic brain injury and that this may produce cerebralischemia As noted above, CPP, which is equal to the MAP minus ICP, is thephysiologic parameter that represents the pressure gradient driving cerebral bloodflow and metabolite/oxygen delivery CPP correlates well with cerebral blood flow

A low CPP correlates with poor outcome in traumatic brain injury patients.Currently, there are no prospective randomized controlled trials (i.e., class I studies)that elucidate the optimal CPP levels in pediatric patients with severe traumaticbrain injury However, several class III studies and one class II study have shownthat a CPP <40 mmHg is associated with decreased survival (32,39) Therefore, inpediatric patients with severe head injury, CPP should be maintained at least above

40 mmHg to prevent regional or global cerebral ischemia

Treatment of Intracranial Hypertension

As noted above, ICP monitoring, with aggressive treatment of intracranial tension and maintenance of adequate CPP/cerebral blood flow (CBF), has led toimproved survival and neurological outcomes after severe traumatic brain injury

hyper-in pediatric patients The goal of ICP management is to reduce the ICP enough toensure an adequate supply of well-oxygenated blood to the brain and prevent ische-mia This requires brain-specific therapies to treat intracranial hypertension as well asthe establishment and maintenance of normal systolic blood pressure and oxygenation

in order to prevent cerebral ischemia and hypoxia during the treatment of intracranialhypertension

As soon as vital signs are stable, the severely head-injured pediatric patientshould undergo cranial CT imaging for accurate diagnosis of intracranial masslesions If a surgical mass lesion is observed on head CT, the patient should be taken

to the operating room immediately for evacuation of the lesion Also, while in theoperating room, an ICP monitor and/or a ventricular drain should be placed ifthe patient’s GCS after resuscitation in the emergency department was 8 and/orthe head CT showed diffuse brain swelling, cisternal effacement, shift, and/or mul-tiple contusions The ventricular drain may be left closed if the ICP is not elevated.The patient should also undergo placement of an arterial line for continuous bloodpressure monitoring and serial arterial blood gas determinations Moreover, thepatient should undergo placement of a central venous line for monitoring centralvenous pressure and for frequent assessment of serum electrolytes, complete bloodcount including hemoglobin and hematocrit, serum osmolarity, and coagulation stu-dies Besides continuous monitoring of blood pressure, central venous pressure, andICP, routine monitoring should include oxygen saturation by means of pulse oxime-try as well as monitoring of temperature, respiratory rate, end-tidal carbon dioxide,and urine output Monitoring of these parameters is essential to the medical manage-ment of pediatric head-injured patients because it allows for the establishment andmaintenance of normal, age-appropriate physiologic parameters and enables promptintervention when deviations occur

At all times during the treatment of intracranial hypertension, the possibilitythat a surgical mass or an unexpected intracranial lesion may have developed should

be reconsidered and the patient should undergo a repeat head CT When intracranialhypertension (defined as ICP greater than 20 mmHg) occurs and there is no surgicalmass lesion evident on head CT, there are several evidence-based treatment strategiesthat can be employed First, physiologic parameters must be optimized For exam-ple, PaO2 should be maintained greater than 80 mmHg and PaCO2 should bemaintained around 35–38 mmHg since hypoxia and hypercarbia cause cerebral vaso-dilatation, which results in increased cerebral blood volume and elevated ICP Inconjunction with this, blood transfusions should be administered as needed to keepthe hemoglobin greater than 11 mg/dL Fluid restriction should be avoided to pre-vent hypovolemia Instead, intravenous isotonic or hypertonic crystalloid solutionsshould be administered in sufficient volumes to maintain a normal or slightlyincreased intravascular volume With regard to temperature control, post-traumatichyperthermia, defined as a core body temperature greater than 38.5C, should beavoided in pediatric patients with severe head injury This is based on data extrapo-lated from studies in animal models and in adult patients with severe head injury (1)

In contrast, a role for therapeutic hypothermia in the treatment of intracranialhypertension in severe pediatric head injury has not been established The patient’s

head should be maintained in a neutral position since rotation of the head or flexion

of the neck can impede jugular venous outflow and increase ICP The endotrachealtube tape and the cervical spine collar should be loosened sufficiently to avoidconstricting jugular venous outflow Finally, as long as the patient is euvolemicand normotensive, the head of the bed can be elevated 15–30 to reduce venous out-flow pressure, which is an effective way to reduce ICP without compromising CPPand cerebral blood flow

Sedatives, Analgesics, and Neuromuscular Blocking Agents

Head-injured patients with intracranial hypertension who have a secure airway andare on mechanical ventilatory support can be treated with sedatives (e.g., benzodia-zepines and barbiturates), analgesics (e.g., narcotics), and neuromuscular blockingagents These medications aid in the management of intracranial hypertension byameliorating agitation, reducing pain and stress, preventing coughing, straining,and shivering, minimizing movement and facilitating assisted ventilation Also, asnoted in the pediatric guidelines sedatives and analgesics can facilitate general care

of the patient in the intensive care unit by helping to maintain the airway,vascular catheters, and other monitors and can facilitate patient transport to theoperating room and for diagnostic procedures (3) However, care must be takenwhen treating patients with sedatives and analgesics because they can cause hypoten-sion Neuromuscular blocking agents can reduce ICP by inhibiting posturing, shiver-ing, and breathing against the ventilator as well as by reducing airway andintrathoracic pressures and thereby improving jugular venous outflow (40) To pre-vent increased stress from immobilization, which can increase ICP, neuromuscularblocking agents should be given in association with adequate sedation and analgesia.Although sedatives, analgesics, and neuromuscular blocking agents are commonlyused in the treatment of pediatric patients with severe head injury, classes I–IIIpediatric studies are currently lacking Therefore, the pediatric guidelines recom-mend at the option level that the treating physician determine the choice and dosing

of these agents (3) However, the continuous infusion of propofol for the purpose ofsedation or management of elevated ICP is not recommended in pediatric patientswith severe traumatic brain injury because it can cause lethal metabolic acidosis(41–43) Moreover, although lidocaine is commonly given in pediatric patients withsevere head injury during suctioning of the endotracheal tube to blunt the reaction toairway stimulation and thereby prevent an increase in ICP, there are no studies in theliterature that evaluate the use of lidocaine for this purpose in pediatric patients.CSF Drainage

If ICP remains elevated despite the aforementioned maneuvers, the ventricular drainmay be opened at 10–15 cm above the external auditory canal for CSF drainage.Ventricular CSF drainage lowers ICP by reducing intracranial fluid volume andhas been shown in a class III study to improve mortality rate in pediatric patientswith severe traumatic brain injury (44) Controlled lumbar drainage of CSF can also

be employed to treat refractory intracranial hypertension in addition to ventriculardrainage when the ventricular drain is functioning adequately and a recent head CTreveals that the basal cisterns are patent and that there are no major intracranialmass lesions or shift (45,46) However, lumbar drainage should be reserved fortreatment of intracranial hypertension that is refractory to the aforementioned

treatment modalities as well as to hyperosmolar therapy (described below) andmild hyperventilation (PaCO230–35 mmHg).

Hyperosmolar Therapy

If intracranial hypertension continues to be elevated after ventricular CSF drainage,one should consider hyperosmolar therapy with intravenous boluses of mannitoland/or continuous infusion of hypertonic saline both of which are effective in themanagement of intracranial hypertension in pediatric patients with severe headinjury (3) Mannitol, which is most effective in controlling ICP when administeredintravenously as intermittent boluses, with doses ranging from 0.25 to 1.0 g/kg ofbody weight, can reduce ICP by at least two mechanisms of action First, as animmediate but transient effect, mannitol changes the rheologic characteristics ofthe blood resulting in decreased viscosity, increased plasma volume, and decreasedhematocrit (47–49) As long as the viscosity autoregulation of cerebral blood flow

is intact, cerebral blood vessels respond to the decrease in blood viscosity by constricting, which decreases cerebral blood volume and thereby reduces ICP Sec-ond, as long as the blood–brain barrier is intact, mannitol has a dehydratingeffect, which results in movement of water from the brain parenchyma into the cir-culation and reduces brain volume (50,51) The osmotic effect of mannitol begins 15–

vaso-30 minutes after mannitol is given and lasts up to six hours Despite the ing and widely accepted use of mannitol in pediatric patients with severe head injury,there currently are no randomized controlled studies that evaluate the efficacy ofmannitol with regard to treatment of intracranial hypertension and long-term neu-rologic outcome in pediatric patients compared with other brain-directed therapies(including other hyperosmolar therapies such as hypertonic saline)

long-stand-Hypertonic saline is also effective in the management of intracranialhypertension in pediatric patients with severe head injury The mechanism of action

of hypertonic saline in reducing ICP is likely similar, at least in part, to that ofmannitol, with both rheologic and osmotic effects playing a role Unlike mannitol,however, hypertonic saline is most effective in reducing ICP when it is administered

as a continuous intravenous infusion of 3% saline at a rate of 0.1–1.0 mL/kg of bodyweight per hour Three class II studies for ICP and one class III study provideevidence supporting the use of 3% saline in the treatment of elevated ICP in pediatricpatients with severe head injury (52–55) These studies demonstrated a reduction inICP in pediatric patients with severe head injury treated with hypertonic saline Two

of these studies also demonstrated a reduced need for additional interventions tocontrol ICP in patients treated with hypertonic saline compared to patients treatedwith 0.9% saline or lactated Ringer’s (54,55) Based on the results of these studies,there is guideline-level support for the use of hypertonic saline in treating intracra-nial hypertension However, as pointed out in the pediatric guidelines clinical experi-ence using hypertonic saline to treat elevated ICP in pediatric patients with severehead injury is limited and the available class II and III studies fail to address theeffect of hypertonic saline on long-term neurologic outcome in severe pediatric headinjury (3) Clearly, further studies are needed to address these issues

When treating elevated ICP with hyperosmolar therapy, such as mannitoland/or 3% saline, it is necessary to maintain the patient in a euvolemic or slightlyhypervolemic status It is also essential to assess frequently the serum electrolytes

as well as the serum osmolarity In order to prevent acute renal failure, the serumosmolarity should not exceed 320 mOsm/L when treating only with mannitol or

360 mOsm/L when treating with 3% saline with or without mannitol Moreover,prophylactic mannitol administration is not recommended unless the patient showssigns of cerebral herniation.

High-Dose Barbiturates

If intracranial hypertension remains refractory despite implementation of theaforementioned management strategies and there is no identifiable cause for ICPintractability noted on repeat head CT, one should consider therapy with high-dosebarbiturates such as pentobarbital or thiopental Treatment of refractory intracra-nial hypertension with high-dose barbiturates reduces ICP by suppressing brainmetabolism and reducing cerebral blood flow and cerebral blood volume (56–58).Based on available data, high-dose barbiturate therapy is supported at the optionlevel for the treatment of medically intractable intracranial hypertension in pediatricpatients with salvageable severe head injury who are stable hemodynamically (3) Incontrast, prophylactic use of barbiturates in pediatric patients early after severe headinjury in an attempt to prevent the development of intracranial hypertension is notsupported currently Moreover, as with many of the other ICP-lowering therapiesalready mentioned, studies demonstrating an improved neurologic outcome inpediatric patients requiring high-dose barbiturate therapy are lacking

Because serum levels of barbiturates do not correlate well with electricalactivity, patients on high-dose barbiturate therapy should undergo continuous elec-troencephalographic monitoring for burst suppression (‘‘barbiturate coma’’), sincethis reflects a near-maximum reduction in brain metabolism and cerebral blood flowand, therefore, a maximum therapeutic effect (56,58) Protocols for treating patientswith high-dose pentobarbital and thiopental have been reported For pentobarbital, aloading dose of 10 mg/kg of body weight is given over a period of 30 minutes, which isfollowed by a 5 mg/kg bolus of pentobarbital every hour for three doses, followed by

a maintenance pentobarbital dose of 1 mg/kg/hr (59) For thiopental, the mended therapeutic regimen consists of a loading dose of 10–20 mg/kg followed

recom-by a maintenance dose of 3–5 mg/kg/hr (60) The maintenance dose is continued

as long as the ICP remains elevated, with the goal of maintaining burst suppression

on the electroencephalogram The barbiturate infusion is continued in this fashionuntil the ICP has been well controlled for at least 24 hours When the ICP is stable,the barbiturate infusion is weaned off gradually Because barbiturates can cause severemyocardial depression, patients on high-dose barbiturates must be monitored carefullyfor hemodynamic instability If hypotension is observed, intravenous fluids and pres-sors must be administered immediately to provide blood pressure support, with the goal

of maintaining it within a normal, age-appropriate range

Hyperventilation

If ICP is still elevated after employing the aforementioned management strategies forreducing ICP, hyperventilation can be considered Hyperventilation, a previouslywidely practiced and long-standing therapy for the treatment of intracranial hyper-tension in both adult and pediatric head-injured patients (e.g., see Ref 61), reducesICP presumably by causing cerebral vasoconstriction and a concomitant reduction

in cerebral blood flow and cerebral blood volume Because of the concern that thisinduced vasoconstriction could cause global or regional ischemia, and thereby con-tribute to the brain injury and worsen neurologic outcome, the adult guidelinesrecommended at the level of treatment standard against the routine use of prolonged

hyperventilation (PaCO2 less than or equal to 25 mmHg) in the management ofhead-injured adult patients (1) It was also recommended at the level of treatmentguideline that prophylactic hyperventilation (PaCO2less than or equal to 35 mmHg)

be avoided during the first 24 hours after head injury (1) To date, no pediatric ies have been conducted that compare the effect of hyperventilation with that ofother ICP-reducing therapies on the outcome of pediatric patients with severe braininjury In the past, aggressive hyperventilation therapy (PaCO2  25 mmHg) wasroutinely employed in the management of intracranial hypertension in pediatricpatients with severe head injury because it was thought that diffuse brain swellingand associated increased ICP were the result of post-traumatic cerebral hyperemia

stud-in these patients (62,63) However, more recent studies have revealed that stud-increasedpost-traumatic cerebral blood flow (i.e., hyperemia) is not a common finding aftersevere pediatric head injury and have raised concerns similar to those in the adulthead-injury literature regarding ischemia from hyperventilation-induced vasocon-striction as a cause of secondary brain injury and worsened neurologic outcome(64,65) As a consequence, the pediatric guidelines make the following recommenda-tions, at the level of treatment options, regarding the use of hyperventilation in themanagement of severe pediatric head injury (3):

1 prophylactic hyperventilation (i.e., PaCO2less than 35 mmHg) should beavoided,

2 mild hyperventilation (i.e., PaCO230–35 mmHg) may be employed to treatintracranial hypertension that fails to respond to other ICP-reducing thera-pies such as sedation, analgesia, neuromuscular blockade, CSF drainage,and hyperosmolar therapy,

3 aggressive hyperventilation therapy (i.e., PaCO2less than 30 mmHg) may

be used for brief periods to treat cerebral herniation or acute neurologicdeterioration as well as to treat medically and surgically intractable intra-cranial hypertension

Decompressive Craniectomy

Another option for treating elevated ICP due to diffuse cerebral swelling that

is refractory to medical management is decompressive craniectomy In pediatricpatients with severe head injury and associated medically intractable intracranialhypertension, decompressive craniectomy has been shown to lower ICP significantlyand have a beneficial effect on neurologic outcome (33,34,66) Commonly emp-loyed operative techniques include unilateral frontal-temporal-parietal-occipitalcraniectomy with expansion duraplasty for cerebral swelling localized to one side

of the brain on head CT and bilateral frontal craniectomy with expansion plasty for diffuse bilateral cerebral swelling In terms of achieving the best possibleoutcome from this procedure, decompressive craniectomy should be performed onsalvageable patients with diffuse cerebral swelling on head CT with secondary clin-ical deterioration or evolving cerebral herniation syndrome who are within 48 hours

dura-of their injury, have a GCS score greater than three, and have not had any longed episodes of ICP elevation greater than 40 mmHg (3,33,34,66)

pro-Anticonvulsants

In pediatric patients with severe head injury, the prophylactic use of anticonvulsantshas not been shown to be beneficial in preventing late post-traumatic seizures or

improving outcome Consequently, the prophylactic use of anticonvulsants inpediatric patients with severe head injury is not recommended In contrast, seizuresdocumented by clinical examination and/or electroencephalogram should be treatedwith anticonvulsants in pediatric patients with severe head injury because seizureactivity can result in significant ICP elevation.

Corticosteroids

Randomized clinical trials evaluating the efficacy of corticosteroids in the ment of severe head injury in adults have shown no significant improvement inthe survival or functional outcome in head-injured adult patients treated with ster-oids (67) The evidence-based guidelines for the management of adult patients withsevere head injury recommend against the routine use of steroids for improving out-come or reducing ICP in the management of adult patients with severe traumaticbrain injury (1) Likewise, there is no role for corticosteroids in the treatment ofpediatric patients with severe traumatic brain injury, even in the face of severe refrac-tory intracranial hypertension In support of this, two class II studies and severalclass III studies (e.g., see Ref 70) have shown that steroids do not reduce ICPand do not improve neurologic outcome in pediatric patients with severe head injury(68,69) Moreover, exogenous steroid administration can suppress the production ofendogenous cortisol and significantly increase the risk of complications such as infec-tion and gastrointestinal hemorrhage (68)

manage-Nutrition

Adult patients with severe head injury commonly become hypermetabolic, withincreased energy expenditure, and are prone to catabolism and nitrogen wasting(71–73) As a consequence, their body energy requirements increase markedly Based

on the significant amount of nitrogen wasting that occurs and the nitrogen sparingeffect of feeding that has been observed in studies on adult patients, the adult guide-lines recommend at the guideline level that nutritional supplementation be institutedwithin 72 hours after the head injury and that full nutritional replacement be in effect

by day seven (1) With regard to energy expenditure and need for nutrition in tric patients with severe head injury, only two previous studies (class II, see Ref 74;class III, see Ref 75) have investigated the need for nutritional support in the treat-ment of pediatric patients with severe head injury These studies revealed a signifi-cant increase in the metabolic rate in pediatric patients with severe head injury butfailed to address the effect of nutritional support on neurologic outcome in thesepatients Nevertheless, based on the data from these two studies, the pediatric guide-lines recommended at the option level that head-injured pediatric patients shouldbegin feedings, either by parenteral or enteral formulas, by 72 hours and should

pedia-be at full replacement (i.e., 130–160% of resting energy expenditure) by seven days(3) Despite the recommendation for early feeding of pediatric patients with severehead injury, the exact role of nutritional supplementation, including the effects oftiming and type, on functional outcome in these patients has not yet been adequatelyinvestigated Consequently, further studies are needed to address these issues More-over, if nutritional supplementation is instituted early in pediatric head injurypatients, blood glucose levels should be monitored frequently and tightly controlled

to prevent hyperglycemia, since previous studies have shown that hyperglycemia canworsen outcome from head injury by exacerbating secondary brain injury (76–78)

To reduce mortality and optimize functional outcome in pediatric patients withsevere head injury, it is necessary to minimize the progression or the effects ofsecondary injury and thereby maximize the potential for recovery Successfulmanagement of severe pediatric head injury requires complete and rapid physiologicresuscitation, which begins with aggressive and organized resuscitation in the field;avoidance of hypotension and hypoxia; prompt diagnosis and removal of intracra-nial mass lesions; aggressive treatment of intracranial hypertension; and mainte-nance of normal physiologic parameters, such as cerebral perfusion, in order tofacilitate adequate delivery of oxygen and metabolic substrates to the brain Atpresent, many questions remain unanswered, especially at the class I level, regardingthe optimal medical and surgical management of severe traumatic brain injury inthe pediatric population Thus, large, well-designed, prospective, randomized, con-trolled multicenter trials are needed to investigate further the effects of differenttreatment modalities on neurologic outcome in order to provide standards of carefor the management of severe pediatric head injury

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