head injury
DESCRIPTION
Paediatric Head InjuryTRANSCRIPT
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NEUROSURGICAL
EMERGENCIES
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NEUROSURGICAL EMERGENCIES
OHead injuryO HydrocephalusO BrainTumoursO Intracranial Bleeds/CVA’sO Shunt complicationsO Spinal cord InjuryO Spinal cord compression and tumours.
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HEAD INJURYO Major cause of mortality and morbidity in
children.O Leading cause of death in children > 1year is
trauma.O Head injury is responsible for most trauma
deaths approximately 80%. (50% in adults)
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PATHOPHYSIOLOGYOChildren are more vulnerable to
injury from head traumaO Relatively large (10% of body weight)
means increased momentum and tend to land on head with falls.
O Elastic, underdeveloped cervical ligaments and muscles are less protective.O Soft calvarium.O Large subarachnoid space (veins at increased risk of tearing)
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ETIOLOGYORoad traffic accidentsSevere head injuriesOFallsUsually in children <4years and usually mildORecreational activitiesBicycle accidentsOAssaults/NAIMost head injuries in kids <1yr are from falls and NAI
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ANATOMYOBRAIN
Inelastic and non compressibleHas no internal support
OCRANIUMRigid and unyielding Bony buttresses at anterior
and temporal polesOMEMBRANOUS “SLINGS”
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Rhoads & Pflanzer (1996) Human Physiology p. 211
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Layers of the Cranial Vault
Anatomy of the Brain www.neurosurgery.org/pubpgages/patres/anatofbrain.
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BRAIN INJURY
Primary
Intracranial HTN
Mass Lesion
Secondary
Delayed cell
death
Ischaemia hypoxia,
hypotension and
hypercarbia
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PRIMARY BRAIN INJURY
Primary
Focal
Coup
Contra coup
Diffuse
DAI
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TRAUMATIC HEAD INJURY
ALL-NET Pediatric Critical Care Textbook Source: LifeART EM Pro (1998) Lippincott Williams & Wilkins. www.med.ub.es/All-Net/english/neuropage/trauma/head-8htm
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TYPES OF PRIMARY INJURY
OFocal injuriesSkull fractureParenchymal contusionParenchymal lacerationVascular injury resulting in epidural,
subdural or parenchymal haematoma.ODiffuse injuries
Diffuse axonal injuryDiffuse vascular injury
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Scalp haematomas/lacerations
OVery vascular, but generally can’t lose enough blood to cause shock or hypovolemia
OCephalohematoma – beneath periosteum (does not cross suture lines)
OSubgaleal bleed - beneath galea (crosses suture lines, often boggy)O Critical in neonate (e.g. from birth trauma)O Can lead to shock/hypovolemia
OClean and examine scalp wounds well to r/o underlying skull fracture; often staple
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SKULL FRACTURES
OANY skull fracture can cause underlying ICH, but 50% of bleeds have no fracture
OSkull films are of little use - if suspect skull fracture or bleed, get non contrast CT
QuickTime™ and a decompressor
are needed to see this picture.
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SKULL FRACTURESOLinear(3/4)- outpatient observation OK,
but get neurosurgical evaluation and f/u if under age 2O Can develop leptomeningeal cyst if dural
tearODepressed - require neurosurgical
evaluation possible repair if depression>skull thicknessO More often develop seizuresO Often get prophylactic AEDs
OBasilar (Battle’s sign, haemotympanum, raccoon eyes) - head CT with inpatient observation, neurosurgical evaluation.
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Case 1
OA 2 year-old comes in after falling approximately 3 feet from her parent’s bed. The CT scan shows the following:
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What is your diagnosis?1. Epidural hematoma2. Subdural hematoma3. Diffuse axonal injury4. Contusion
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Subdural
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Subdural HematomaOMore common than
epidural in childrenOTears in parasagittal
bridging veinsOConcave shapeOOften associated with
more diffuse shear injury
O Immediate surgical tx if pt is unconscious and has subdural bleed
OSuspect NAI
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Case 2
OA 5 year old girl falls from a second story window. You find the following on CT scan:
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What is your diagnosis?
1. Epidural hematoma2. Subdural hematoma3. Diffuse axonal injury4. Contusion
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Epidural Hematoma
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Epidural HematomaOCaused by tears of
meningeal vesselsOConvex shapeOOften associated bone
fracture (up to 75%)OTypically few hours of
lucidity followed by rapid deterioration
ONeed close observation and often surgical evacuation
OGood prognosis if recognized and treated
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SUBDURAL VS. EPIDURAL
LifeArt: Williams & Wilkinshttp://www.lifeart.com
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SUBDURAL HEMATOMA
WebPath: University of Utahhttp://www-medlib.med.utah.edu
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EPIDURAL HEMATOMA
WebPath: University of Utahhttp://www-medlib.med.utah.edu/
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SUBDURAL vs EPIDURAL HEMATOMA
OEPIDURALO Requires linear
forceO Associated with
skull fracture and torn artery. Brain often uninjured
O “Lucid” interval common
O Common in accidental trauma
OSUBDURALO Requires
significant rotational forces
O Associated with brain injury and torn bridging veins
O Neurologic symptoms from the start
O Common in infants with NAI.
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Cerebral Contusion
OOccur at the site of blunt traumaOUsually have loss of consciousnessOCan be very small/mild or large,
resulting in significant symptoms (cerebral edema, increased ICP)
OOften associated with intracranial hematomas or skull fractures
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Intracerebral Haemorrhage
ORare in Paediatric population.OUsually frontal or temporal lobeOCan be bilateral(countracoup injury)OCan act as mass lesions and cause
intracranial hypertensionOCT-Hyperdense/mixedOMRI-Small petechia+DAIORx: Small-non operative Large-Sx drainage
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Penetrating Head InjuryO Infants and children: fall on sharp objects, NAI,
GSWO CT- Localizes bullet and bone fragments.O MRI-Not advised till magnetic properties of bullet
knownO Treatment: Debridement of entry and exit wounds Remove accessible bullet and bony fragments Control haemorrhage Repair dural lacerations+closure of wounds No attempt to REMOVE BULLET OR BONE beyond
entry and exit wounds.
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Diffuse Axonal Injury
OOften from acceleration/deceleration injuries (RTA, falls, shaking)
OWidespread shearing of white matter
OSuspect if patient has subarachnoid bleeding and cerebral edema
OEdema develops over 24-48 hours
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• Shearing injury of axons • Deep cerebral cortex, thalamus, basal
ganglia• Punctate hemorrhage and diffuse
cerebral edema
Image from: Neuroscience for Kids www.faculty.washington.edu/chudler/cells/html
Diffuse Axonal Injury
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Secondary InjuryO Subsequent factors that secondarily cause
brain tissue damageO Intracranial
O Hemorrhage/IschemiaO EdemaO Increased ICP
O SystemicO Hypoxia/hypercapniaO HypotensionO Hyperglycemia
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Assessment of severity
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Defining SeverityOMild Brain Injury
OGCS = 13-15OLimited impaired consciousness (<30 min)ONormal CT scanOShows signs of a concussion
OVomitingOLethargyODizzinessOLacks recall about injury
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Defining SeverityOModerate Brain Injury
OGCS = 9 - 12O Impaired Consciousness (<24)OCT scan Evidence
OSevere Brain InjuryOGCS = 3 - 8O Impaired Consciousness
(> 24 hours)
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CAUTION!!
OGCS of 13 may not be so “mild”
OSC Stein, J Trauma. 2001;50:759-760OReviewed 14 studies (1047 adult patients with GCS of 13) O33.8% had intracranial lesionsO10.8% required surgery
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Defining Severity
OGCS, hypoxemia and radiologic evidence of SAH, cerebral edema and DAI are predictive of morbidity.
OGCS alone does not predict morbidity. Ong et al. (1996) Pediatric Neurosurgery, 24(6)
OHypotension is predictive of morbidity.OGCS and Pediatric Trauma Score are
not predictive of outcome. Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)
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CT or no CTO A 3months old baby presented with
minor head injury. Fell of the table about 2 feet high. NO LOCGCS 15
O/E well, pupils b/l equal and reacting 6 cm laceration occipital area
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CT or no CTO 15 year old boy football injury.
Brief LOC Vomited once at scene
O/EWell, alert, GCS 15
No focal neurology
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Admission or no Admission
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Admission or no Admission
O 15 year old boy hit by car.O GCS 14/15 E 4 M6 V4O Rest all ok!
CT or no CT?Admission?Neuro obs:
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Head injurytriage, assessment, investigation and early management of head injury in infants, children and adults (update)
Implementing NICE guidance
December 2007
NICE clinical guideline 56
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Updated guidanceO This guideline replaces ‘Head injury: triage,
assessment, investigation and early management of head injury in infants, children and adults’ (NICE clinical guideline 4, 2003)
O There was sufficient new evidence to prompt an update to be carried out which means changes in clinical practice
O There are new and amended recommendations
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Key recommendationsO Initial assessment in the emergency department
O Urgency of imaging
O Admission• Criteria for admission• When to involve the neurosurgeon
O Organisation of transfer of patients between
referring hospital and neuroscience unit
O Advice about long-term problems and support services
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Initial assessment in the emergency department (ED)
O All patients presenting to an ED with a head injury should be assessed by a trained member of staff within 15 minutes of arrival at hospital
O This assessment should establish whether they are high risk or low risk for clinically important brain injury and/or cervical spine injury
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Urgency of imaging: head CT OCT of the head should be performed and
analysed within 1 hour of imaging request in patients who have any of these risk factors:
OGlasgow Coma Scale (GCS) < 13 on initial assessment in A&E or < 15 at 2 hours after injury
OSuspected open or depressed skull fracture or any sign of basal skull fracture
OTwo or more episodes of vomiting in adults; three or more in children
OPost-traumatic seizure
OCoagulopathy, providing that some loss of consciousness or amnesia has been experienced
OFocal neurological deficit
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Urgency of imaging: head CT
O Patients who have any of the risk factors below, and none of the risk factors on the previous slide should have CT imaging of the head performed within 8 hours of the injury:O Amnesia for > 30 minutes of events before impact
(assessment unlikely to be possible in any child aged under 5 years)
O Age 65 years, providing that some loss of consciousness or amnesia has been experienced
O Dangerous mechanism of injury (e.g. a fall from a height of > 1 metre or 5 stairs), providing that some loss of consciousness or amnesia has been experienced.
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Admission: Criteria
O Clinically significant abnormalities on imaging
O Patient has not returned to GCS 15 after imaging, regardless of the imaging results
O Criteria for CT scanning fulfilled, but scan not done within appropriate period, either because CT not available or because patient not sufficiently cooperative to allow scanning
O Continuing worrying signs (e.g. persistent vomiting)
O Other sources of concern (e.g. drug intoxication, other injuries, non accidental injury)
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Secondary Brain InjuryPotentially Avoidable Or Treatable With Close Monitoring / Treatment of ABC’s
O HypoxiaO HypercarbiaO Hypotension/ischemiaO Intracranial hypertensionO Acidosis O SeizuresO HyperthermiaO HypothermiaO Infections
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Evidence based management of severe traumatic brain injury in children
O Guidelines for the Acute Medical Management of severe traumatic Brain Injury in infants, Children, and Adolescents.
Journal of Pediatric Critical Care Medicine. January 2012-Second edition
O Text book of Paediatric critical care Bradley P.Fuhrman, Jerry J.Zimmerman Third edition2006
O NICE Guidelines- Updated December 2007
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Level of EvidenceOLevel I Good quality RCT
OLevel II Moderate or poor quality RCT Good quality cohort Good quality case control
OLevel III Moderate or poor quality RCT or cohort Moderate or poor quality case control Case series, databases, registeries
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INITIAL MANAGEMENTOAIRWAY with C-Spine control
OBREATHING
OC T SCAN CIRCULATION
ODOEOF & G
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EARLY RESUSCITATION OF CHILDREN WITH MODERATE-TO-SEVERE TRAUMATIC BRAIN
INJURY PEDIATRICS 2009;124;56-64 MICHELLE ZEBRACK, CHRISTOPHER DANDOY, KRISTINE HANSEN, ERIC SCAIFE, N. CLAY MANN AND SUSAN L. BRATTON
O CONCLUSIONS: Hypotension and hypoxia are common events in pediatric traumatic brain injury. Approximately one third of children are not properly monitored in the early phases of their management. Attempts to treat hypotension and hypoxia significantly improved out-comes.
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Circulatory Support: Maintain Cerebral Perfusion Pressure
0
1
2
3
4
5
6
Patient Outcome
Good
Moderate
Severe
Vegetative
Dead
Number of Hypotensive Episodes in the first 24 hours after TBI
Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)
CPP = MAP - ICP
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Airway and ventilationCriteria for the intubation of Head injured
childO GCS<10O Decrease in GCS of >3, independent of the
initial GCS.O Anisocoria>1mmO Cervical spine injury compromising
ventilation.O ApnoeaO Hypercarbia(PaCo2>45mmg/6.0Kpa)O Loss of pharyngeal reflexO Spontaneous hyperventilation causing
PaCo2<25mmHg/3.3Kpa
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Airway and ventilationO Hypoxia to be avoided. Aim Pao2 of >13kpa Aim PaCo2 of 4.5-5.0kpa
O Avoidance of prophylactic severe hyperventilation to a PaCO2 of <30mmHg(4.0kpa).
O If hyperventilation is used in the management of refractory intracranial hypertension, advanced neuromonitoring like
jugular venous oxygen saturations, brain tissue oxygen tension measurements
for evaluation of cerebral ischemia may be considered.
(LEVEL III)
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Head elevation of 30 degrees
OThis improves venous drainage with minimal effect on arterial pressure.
OHead in midline to ensure no pressure or kinking of neck veins.
O If head raised more then 30 degrees possible adverse effect on cerebral arterial pressure.
Carter BG, Butt W, Taylor A: ICP and CPP: Excellent predictors of long term outcome in severely brain injured children. Childs Nerv Syst 2008; 24:245–251
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Keep neck mid-line and elevate head of bed …. To what degree?Feldman et al. (1992) Journal of Neurosurgery, 76
March et al. (1990) Journal of Neuroscience Nursing, 22(6)
Parsons & Wilson (1984) Nursing Research, 33(2)
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Normal Cerebral MetabolismOBrain tissue relies on aerobic
metabolism.
ONormal cerebral metabolism requires a blood flow of approximately 50 mL/100g/min.
OSerious neurological deficits begin to occur at 20 mL/100g/min.
OProlonged Cerebral Blood Flow < 12 mL/100g/min. results in cerebral infarction.
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CBF AutoregulationO CBF maintained within CPP range of 50 – 150 mmHg.O CPP =MAP – ICPO <50 CPP= Maximal dilation CBF fallsO >150 CPP=Maximal constric CBF raisesAutoregulation 1)Completely lost-linear relation CBF & CPP2)Incompletely lost-Plateau after CPP of 80 mmHg
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Copied from: Rogers (1996) Textbook of Pediatric Intensive Care p. 646
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ICP Monitoring-Level III
O A frequently reported high incidence of intracranial hypertension in children with severe TBI.
O A widely reported association of intracranial hypertension and poor neurologic outcome
O The concordance of protocol-based intracranial hypertension therapy and best-reported clinical outcomes
O Improved outcomes associated with successful ICP-lowering therapies
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Monitoring of Intracranial pressure
O Indications: GCS <8 Abnormal head CT Rapid neurological deteriorationNormal CT head in adultsO Age>40O Unilateral or bilateral motor posturingO Systolic BP <90
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Treatment of raised ICPOTreatment of intracranial pressure (ICP)
may be considered at a threshold of 20 mm Hg (LEVELIII).
Grinkeviciute DE, Kevalas R, Matukevicius A, et al.: Significance of intracranial pressure and cerebral perfusion pressure in severe pediatric traumatic brain injury. Medicina (Kaunas, Lithuania) 2008; 44:119–125
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Cerebral perfusion pressure
OA minimum CPP OF 40mmHg (Level III) may be considered in children with TBI.
OA CPP threshold of 40-50mmHg may be considered; infants at lower end and adolescents at the upper end of this range.
(Level III).
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ICP Measurement-InvasiveO Intraventricular catheter coupled to ICP
transducer is Gold standard. Adv: CSF can be drained Dis adv: Infection, Ventricular compression leads to inaccuracyO Fiberoptic cath: Adv: Improved Longevity, can be placed intraparenchymal/intraventricular/subdural Dis adv: Not able to drain CSFO Subdural/subarachnoid Bolts: Occulusion of ports can lead to inaccuracy
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Advanced Neuromonitoring
OIf brain oxygenation monitoring is used, maintenance of partial pressure of brain tissue oxygen (PbtO2) >10 mm Hg may be considered.(LEVEL III)
O Figaji AA, Zwane E, Thompson C, et al.: Brain tissue oxygen tension monitoring in pediatric severe traumatic brain injury. Part 1: Relationship with outcome. Childs Nerv Syst 2009; 25:1325–1333
O Narotam PK, Burjonrappa SC, Raynor SC, et al.: Cerebral oxygenation in major pediatric trauma: its relevance to trauma severity and outcome. J Pediatr Surg 2006; 41:505–513
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Neuroimaging
O In the absence of neurologic deterioration or increasing intracranial pressure (ICP), obtaining a routine repeat computed tomography (CT) scan >24hrs after the admission and initial follow-up study may not be indicated for decisions about neurosurgical intervention. (LEVEL III)
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Hyperosmolar therapy
O Hypertonic saline should be considered for the treatment of severe paediatric traumatic brain injury associated with intracranial hypertension. Effective doses for acute use range between 6.5 and 10 mL/kg (of 3%) (LEVEL II).
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Temperature controlO Moderate hypothermia (32–33°C) beginning
early after severe traumatic brain injury (TBI) for only 24hr’s duration should be avoided
O Moderate hypothermia (32–33°C) beginning within 8 hrs after severe TBI for up to 48 hrs’ duration should be considered to reduce intracranial hypertension.
O If hypothermia is induced for any indication, rewarming at a rate of >0.5°C/hr should be avoided (LEVEL II).
O Moderate hypothermia (32–33°C) beginning early after severe TBI for 48 hrs, duration may be considered (LEVEL III).
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Cerebrospinal fluid drainageO Cerebrospinal fluid (CSF) drainage through an
external ventricular drain may be considered in the management of increased intracranial pressure (ICP) in children with severe traumatic brain injury (TBI).
O The addition of a lumbar drain may be considered in the case of refractory intracranial hypertension with a functioning external ventricular drain, open basal cisterns, and no evidence of a mass lesion or shift on imaging studies (LEVEL III).
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BarbituratesO High-dose barbiturate therapy may be
considered in haemodynamically stable patients with refractory intracranial hypertension despite maximal medical and surgical management.
O When high-dose barbiturate therapy is used to treat refractory intracranial hypertension, continuous arterial blood pressure monitoring and cardiovascular support to maintain adequate cerebral perfusion pressure are required (LEVEL III).
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Decompressive craniectomy
O Decompressive craniectomy (DC) with duraplasty, leaving the bone flap out, may be considered for paediatric patients with TBI who are showing early signs of neurologic deterioration or herniation or are developing intracranial hypertension refractory to medical management during the early stages of their treatment.
(LEVEL III).
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CorticosteroidsO The use of corticosteroids is not
recommended to improve outcome or reduce intracranial pressure (ICP) for children with severe traumatic brain injury.(LEVEL III)
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Analgesics, sedatives, and neuromuscular blockade
OThiopental may be considered to control intracranial hypertension.
OPropofol Not recommended.(LEVEL III)OEtomidate can be used as a one off bolus but look for adrenal suppression.
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Before During After
TurningSuctioningBathing
Nursing Activities and ICP
Rising (1993) Journal of Neuroscience Nursing, 25(5)
ICP
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Glucose and nutrition
O The evidence does not support the use of an immune-modulating diet for the treatment of severe traumatic brain injury (TBI) to improve outcome (LEVEL II).
O In the absence of outcome data, the specific approach to glycemic control in the management of infants and children with severe TBI should be left to the treating physician (LEVEL III)
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Antiseizure prophylaxis
O Prophylactic treatment with phenytoin may be considered to reduce the incidence of early posttraumatic seizures (PTS) in paediatric patients with severe TBI (LEVEL III).
O The incidence of early PTS in paediatric patients with TBI is approximately 10% given the limitations of the available data. Based on a single class III study, prophylactic anticonvulsant therapy with phenytoin may be considered to reduce the incidence of early posttraumatic seizures.
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Questions?
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SummaryOSerial neurologic assessments and
physical examinationOContinuous cardio-respiratory, ICP,
and CPP monitoring, +/- cerebral metabolism monitoring adjuncts
OMaximize Oxygenation and Ventilation Maximize oxygenation Normo-ventilate Support circulation / maximize cerebral perfusion
pressure Maintain mean arterial blood pressure and maintain CPP.
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SummaryODecrease intracranial pressure
O Evacuate mass occupying hemorrhages/lesions.
O Consider draining CSF when possibleO Hyperosmolar therapy, cautious use to
avoid hypovolemia and decreased BPO Mid-line neck, elevated head to 30
degree.O Treat pain and agitation - consider pre-
medication for nursing activities, +/- neuromuscular blockade.
O Careful monitoring of ICP during nursing care, cluster nursing activities and limit handling when possible
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Summary
ODecrease Cerebral Metabolic RateO Prevent seizures O Reserve thiopentone for refractory
conditionsO Avoid hyperthermia, +/- hypothermiaO Avoid hyperglycemia (early)