UTHSCSA Pediatric Resident Curriculum for the PICU HEAD INJURY AND INTRACRANIAL HYPERTENSION

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HEAD INJURY AND HEAD INJURY AND INTRACRANIAL INTRACRANIAL HYPERTENSIONHYPERTENSION

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HEAD INJURYHEAD INJURY• Major cause of morbidity and mortality in Major cause of morbidity and mortality in

childrenchildren• Leading cause of death in children > 1 yr is Leading cause of death in children > 1 yr is

traumatrauma• Head injuries responsible for most trauma Head injuries responsible for most trauma

deathsdeaths• Adverse outcomes result fromAdverse outcomes result from

– Primary injuryPrimary injury• Result of mechanical forces producing Result of mechanical forces producing

tissue deformation at the moment of tissue deformation at the moment of injuryinjury

– Secondary ischemic injurySecondary ischemic injury• Associated with post injury hypotension, Associated with post injury hypotension,

hypoxemia, and intracranial hypertensionhypoxemia, and intracranial hypertension

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ETIOLOGIESETIOLOGIES

• Motor vehicle accidentsMotor vehicle accidents– Responsible for most severe head Responsible for most severe head

injuriesinjuries• FallsFalls

– Usually in children < 4 yrs and usually Usually in children < 4 yrs and usually mildmild

• Recreational activitiesRecreational activities– Half of these are bicycle accidentsHalf of these are bicycle accidents

• Assault or nonaccidental traumaAssault or nonaccidental trauma– Most head injuries in kids < 1 yr are Most head injuries in kids < 1 yr are

from NAT and fallsfrom NAT and falls

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ANATOMYANATOMY• Uniquely susceptible to injuryUniquely susceptible to injury• BrainBrain

– Inelastic and noncompressibleInelastic and noncompressible– Has no internal supportHas no internal support

• CraniumCranium– Rigid and unyielding after sutures fusedRigid and unyielding after sutures fused– Bony buttresses at anterior poles and Bony buttresses at anterior poles and

temporal polestemporal poles• Membranous “slings”Membranous “slings”

– Falx cerebri compartmentalizes R and L Falx cerebri compartmentalizes R and L hemisphereshemispheres

– Tentorium separates infra- and Tentorium separates infra- and supratentorial regionssupratentorial regions

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MECHANISM OF BRAIN INJURYMECHANISM OF BRAIN INJURY

• Brain is thrown against bony Brain is thrown against bony irregularities or membranous slings or irregularities or membranous slings or compressed against these surfaces compressed against these surfaces by…by…– Contact injuryContact injury

• Head strikes or is struck by an Head strikes or is struck by an objectobject

– Acceleration/deceleration injuryAcceleration/deceleration injury• Violent head motion causes Violent head motion causes

compressive, tensile, and shear compressive, tensile, and shear strain in brain tissuestrain in brain tissue

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ICU COUP - CONTRECOUP COUP - CONTRECOUP

INJURYINJURY

LifeArt: Williams & WilkinsLifeArt: Williams & Wilkinshttp://www.lifeart.comhttp://www.lifeart.com

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TYPES OF PRIMARY INJURIESTYPES OF PRIMARY INJURIES

• Diffuse injuriesDiffuse injuries– Diffuse axonal Diffuse axonal

injuryinjury– Diffuse vascular Diffuse vascular

injuryinjury

• Focal injuriesFocal injuries– Skull fractureSkull fracture– Parenchymal Parenchymal

contusioncontusion– Parenchymal Parenchymal

lacerationlaceration– Vascular injury Vascular injury

resulting in resulting in hematoma hematoma (subdural, (subdural, extradural, or extradural, or parenchymal)parenchymal)

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SKULL FRACTURESSKULL FRACTURES

• Most are uncomplicatedMost are uncomplicated• Basilar skull fracturesBasilar skull fractures

– Battles sign, “raccoon eyes”Battles sign, “raccoon eyes”– CSF rhinorrhea, CSF otorrhea possibleCSF rhinorrhea, CSF otorrhea possible– Cranial nerve injury possibleCranial nerve injury possible

• Depressed skull fractures represent more severe Depressed skull fractures represent more severe injuryinjury– 1/3 are associated with dural laceration1/3 are associated with dural laceration– 1/3 are associated with cortical laceration1/3 are associated with cortical laceration– May require surgical elevationMay require surgical elevation

• Fracture crossing path of major vascular structure Fracture crossing path of major vascular structure increases risk for significant bleedingincreases risk for significant bleeding– Middle meningeal arteryMiddle meningeal artery– Large dural sinusLarge dural sinus

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•Usually frontal or Usually frontal or temporal lobetemporal lobe•Small cortical Small cortical vessels and neural vessels and neural tissue damagedtissue damaged•Damaged vessels Damaged vessels may thombose, may thombose, leading to ischemialeading to ischemia

CONTUSIONCONTUSION

WebPath: University of UtahWebPath: University of Utahhttp://www-medlib.med.utah.edu/WebPath/webpath.htmlhttp://www-medlib.med.utah.edu/WebPath/webpath.html

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•Usually frontal or Usually frontal or temporal lobetemporal lobe•Can be bilateral Can be bilateral (contracoup injury)(contracoup injury)•Can act as mass Can act as mass lesions and cause lesions and cause intracranial intracranial hypertensionhypertension

INTRACEREBRAL INTRACEREBRAL HEMORRHAGEHEMORRHAGE

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•Usually arterial in originUsually arterial in origin•Between skull and dura, Between skull and dura, limited by suture lineslimited by suture lines•Often from tear in middle Often from tear in middle meningeal arterymeningeal artery•Initial injury may seem Initial injury may seem minor, followed by “lucid minor, followed by “lucid interval,” then neurologic interval,” then neurologic deteriorationdeterioration•May expand rapidly and May expand rapidly and require emergency require emergency craniotomy craniotomy

EPIDURAL HEMATOMAEPIDURAL HEMATOMA


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•Usually venous bleeding Usually venous bleeding (bridging veins)(bridging veins)•On surface of cortex, beneath On surface of cortex, beneath dura and outside arachnoid, not dura and outside arachnoid, not limited by suture lines.limited by suture lines.•Typically requires greater force Typically requires greater force to produce than epidural to produce than epidural hematomahematoma•Usually associated with severe Usually associated with severe parenchymal injuryparenchymal injury

SUBDURAL HEMATOMASUBDURAL HEMATOMA


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DIFFUSE BRAIN INJURYDIFFUSE BRAIN INJURY

• Diffuse axonal injuryDiffuse axonal injury– Usually from rapid acceleration/decelerationUsually from rapid acceleration/deceleration– Shear forces disrupt small axonal pathwaysShear forces disrupt small axonal pathways

• After disruption, axons degenerate, fragment, After disruption, axons degenerate, fragment, then disappearthen disappear

• The neurons then undergo Wallerian The neurons then undergo Wallerian degenerationdegeneration

– Spectrum from mild to severeSpectrum from mild to severe• Diffuse vascular injuryDiffuse vascular injury

– Microvasculature more resistant to shear than Microvasculature more resistant to shear than axonsaxons

– Results in multiple small hemorrhages Results in multiple small hemorrhages throughout brainthroughout brain

– Usually seen in fatal head injuriesUsually seen in fatal head injuries

. ...... . ..

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SECONDARY ISCHEMIC SECONDARY ISCHEMIC BRAIN INJURYBRAIN INJURY

• Compounds the potential for adverse Compounds the potential for adverse neurologic outcomeneurologic outcome

• Caused by:Caused by:– Post injury hypotensionPost injury hypotension– HypoxemiaHypoxemia– Intracranial hypertension which Intracranial hypertension which

impairs cerebral bloodimpairs cerebral blood flowflow

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ICU INTRACRANIAL INTRACRANIAL

HYPERTENSIONHYPERTENSION• Vascular etiologiesVascular etiologies

– Vasogenic edema Vasogenic edema • BBB impaired, BBB impaired,

protein rich fluid protein rich fluid leaks to ECFleaks to ECF

– Hyperemia Hyperemia • Occurs days 1 to 3 Occurs days 1 to 3

after injuryafter injury– Obstructed venous Obstructed venous

drainagedrainage• Hydrostatic Hydrostatic

pressure increased, pressure increased, protein poor fluid protein poor fluid leaks into ECFleaks into ECF

• Nonvascular etiologiesNonvascular etiologies– Cytotoxic edemaCytotoxic edema

• Ionic gradients Ionic gradients impaired and cells impaired and cells swellswell

– Obstruction to CSF Obstruction to CSF outflowoutflow

– HematomaHematoma– Osmotic brain edemaOsmotic brain edema

• Decreased Decreased osmolality from osmolality from iatrogenic iatrogenic hemodilution or hemodilution or SIADHSIADH

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ICU INTRACRANIAL INTRACRANIAL

HYPERTENSIONHYPERTENSION• Normal intracranial pressure:Normal intracranial pressure:

– Adults: < 10 mm HgAdults: < 10 mm Hg– Infants/children: somewhat lower, Infants/children: somewhat lower,

depending on agedepending on age• Elevated ICP impairs cerebral Elevated ICP impairs cerebral

perfusionperfusion• Risk for herniation with ICP > 40 mm Risk for herniation with ICP > 40 mm

HgHg• Herniation can occur at lower ICP’s Herniation can occur at lower ICP’s

when mass lesion is presentwhen mass lesion is present

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ICU MANAGEMENT OF HEAD MANAGEMENT OF HEAD

INJURYINJURY• Goals of resuscitation and treatment Goals of resuscitation and treatment

is to minimize secondary ischemic is to minimize secondary ischemic brain injury by promoting and brain injury by promoting and preserving cerebral perfusionpreserving cerebral perfusion– Prevent or treat post injury hypotensionPrevent or treat post injury hypotension– Prevent or treat hypoxemia and reduce Prevent or treat hypoxemia and reduce

oxygen demand of the brain oxygen demand of the brain – Prevent or treat intracranial Prevent or treat intracranial

hypertensionhypertension– Avoid measures that decrease cerebral Avoid measures that decrease cerebral

perfusionperfusion

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RESUSCITATIONRESUSCITATION

• A, B,C’sA, B,C’s• Major early risk is hypotensionMajor early risk is hypotension

– Adequate fluid resuscitation to restore Adequate fluid resuscitation to restore normal BP does NOT worsen neurologic normal BP does NOT worsen neurologic outcomeoutcome

– Avoid hypotonic fluidsAvoid hypotonic fluids• Emergent airway control forEmergent airway control for

– GCS 8 or lessGCS 8 or less– GSC 10 or less with abnormal head CTGSC 10 or less with abnormal head CT– Rapid neurologic deteriorationRapid neurologic deterioration– If needed for other injuriesIf needed for other injuries

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INTUBATION OF PATIENT WITH INTUBATION OF PATIENT WITH HEAD INJURYHEAD INJURY

• Preserve cerebral oxygenationPreserve cerebral oxygenation• Maintain cerebral perfusionMaintain cerebral perfusion

– Adequate analgesia and anxiolysisAdequate analgesia and anxiolysis– Avoid meds that increase ICPAvoid meds that increase ICP– Avoid meds that cause hypotension Avoid meds that cause hypotension – Avoid Trendelenburg positionAvoid Trendelenburg position

• Avoid aggravating C spine injuryAvoid aggravating C spine injury– C-spine injuries in as many as 10% of C-spine injuries in as many as 10% of

head injury patientshead injury patients– In-line axial stabilization by an assistant In-line axial stabilization by an assistant

recommendedrecommended

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DRUGS FOR RAPID DRUGS FOR RAPID SEQUENCE INTUBATIONSEQUENCE INTUBATION

• Analgesia/sedationAnalgesia/sedation– Fentanyl, etomidateFentanyl, etomidate

• little effect on BPlittle effect on BP– ThiopentalThiopental

• decreases ICP but decreases ICP but can drop BPcan drop BP

• AnxiolysisAnxiolysis– MidazolamMidazolam

• little effect on BPlittle effect on BP• Lidocaine IVLidocaine IV

• blunts sympathetic blunts sympathetic response to response to intubationintubation

• Neuromuscular blockadeNeuromuscular blockade– Succinyl cholineSuccinyl choline

• short actingshort acting• muscle fasciculations muscle fasciculations

can increase ICPcan increase ICP• use with use with

defasciculating dose defasciculating dose of nondepolarizingof nondepolarizing

– Non depolarizingNon depolarizing• vecuroniumvecuronium• longer acting and no longer acting and no

increase in ICPincrease in ICP

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RULE OUT & PREVENT NEUROSURGICAL RULE OUT & PREVENT NEUROSURGICAL EMERGENCIESEMERGENCIES

• Head CT as soon as possibleHead CT as soon as possible– Initial CT may be normal in severe Initial CT may be normal in severe

head injuryhead injury– Repeat CT in 12 to 24 hoursRepeat CT in 12 to 24 hours

• Moderate hyperventilation advisable Moderate hyperventilation advisable during transport and initial evaluationduring transport and initial evaluation

• If signs of impending herniation develop If signs of impending herniation develop (lateralizing signs, pupil asymmetry)(lateralizing signs, pupil asymmetry)– HyperventilateHyperventilate– Give mannitolGive mannitol

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MONITORING OF INTRACRANIAL MONITORING OF INTRACRANIAL PRESSUREPRESSURE

• Ventriculostomy catheterVentriculostomy catheter– Catheter tip in frontal horn of lateral Catheter tip in frontal horn of lateral

ventricleventricle– Can drain CSFCan drain CSF– Can be recalibrated as necessaryCan be recalibrated as necessary

• Transducer tipped catheterTransducer tipped catheter– Intraparenchymal or subduralIntraparenchymal or subdural– Cannot drain CSFCannot drain CSF– Cannot be recalibratedCannot be recalibrated– Exhibits drift in values measured over Exhibits drift in values measured over

timetime

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MONITORING OF INTRACRANIAL MONITORING OF INTRACRANIAL PRESSUREPRESSURE

• IndicationsIndications– GCS < 8 after resuscitationGCS < 8 after resuscitation– Abnormal head CTAbnormal head CT– Rapid neurologic deteriorationRapid neurologic deterioration

• ICP monitoring is continued for ICP monitoring is continued for as long as treatment of as long as treatment of intracranial hypertension is intracranial hypertension is requiredrequired

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CEREBRAL PERFUSION CEREBRAL PERFUSION PRESSUREPRESSURE

• Can be determined from ICP and mean Can be determined from ICP and mean arterial pressure:arterial pressure:

CPP = MAP - ICPCPP = MAP - ICP• Calculated CPP does not reflect perfusion Calculated CPP does not reflect perfusion

of entire brainof entire brain– CPP further decreased in areas of CPP further decreased in areas of

injuryinjury– Factors that cause cerebral Factors that cause cerebral

vasoconstriction without lowering MAP vasoconstriction without lowering MAP result in a falsely low calculated CPPresult in a falsely low calculated CPP

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CEREBRAL PERFUSION CEREBRAL PERFUSION PRESSUREPRESSURE

• Goal of therapyGoal of therapy CPP > 60 mm Hg if ICP < 22 mm HgCPP > 60 mm Hg if ICP < 22 mm Hg

oror CPP > 70 mm Hg if ICP > 22 mm HgCPP > 70 mm Hg if ICP > 22 mm Hg

– Lowering ICP while maintaining MAP Lowering ICP while maintaining MAP will increase CPPwill increase CPP

– Increasing MAP will increase CPPIncreasing MAP will increase CPP

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FACTORS AFFECTING FACTORS AFFECTING INTRACRANIAL PRESSUREINTRACRANIAL PRESSURE

• Increases ICPIncreases ICP– hypercarbiahypercarbia– hypoxia (pOhypoxia (pO2 2 < 50)< 50)– seizures or seizures or

shiveringshivering– hyperthermiahyperthermia– arousalarousal

• pain, anxietypain, anxiety– venous congestionvenous congestion

• fluid overloadfluid overload• intrathoracic intrathoracic

pressurepressure

• Decreases ICPDecreases ICP– hyperoxiahyperoxia– hypothermiahypothermia– barbituratesbarbiturates– hypocapniahypocapnia

• via cerebral via cerebral vasoconstrictiovasoconstrictionn

• lowers CPP and lowers CPP and is undesirableis undesirable

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EFFECT OF pCOEFFECT OF pCO22 and pO and pO22 ON ON CBF AND CPPCBF AND CPP

• Hypoxia increases Hypoxia increases CBF by vasodilationCBF by vasodilation

• Hypercapnia Hypercapnia increases CBFincreases CBF

• Hyperventilation and Hyperventilation and resulting hypocapnia resulting hypocapnia decrease CBFdecrease CBF– Hyperventilation is Hyperventilation is

useful to prevent useful to prevent impending impending herniation but will herniation but will worsen secondary worsen secondary ischemic injuryischemic injury

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MANAGEMENT OF MANAGEMENT OF INCREASED ICPINCREASED ICP

• Head positionHead position– Head elevated 30 degrees and midlineHead elevated 30 degrees and midline

• Sedation and pain controlSedation and pain control– Analgesic + anxiolyticAnalgesic + anxiolytic

• Fentanyl, morphine, or propofol plus Fentanyl, morphine, or propofol plus a benzodiazepinea benzodiazepine

• Continuous infusions or scheduled Continuous infusions or scheduled doses to maintain sedationdoses to maintain sedation

– Watch for and treat hypotensionWatch for and treat hypotension• Seizure prophylaxisSeizure prophylaxis

– Phenytoin or phosphenytoinPhenytoin or phosphenytoin

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MANAGEMENT OF INCREASED MANAGEMENT OF INCREASED ICPICP

• Neuromuscular blockadeNeuromuscular blockade– Facilitates mechanical ventilation and Facilitates mechanical ventilation and

control of pCOcontrol of pCO22

– Prevents shiveringPrevents shivering– Use if movement increases ICPUse if movement increases ICP

• Temperature controlTemperature control– A rise in temp of 1A rise in temp of 1oo C increases cerebral C increases cerebral

metabolic rate by 10%, increasing ICP by metabolic rate by 10%, increasing ICP by several mm Hgseveral mm Hg

– Maintain temp < 37.5 Maintain temp < 37.5 oo C C• Scheduled acetaminophen, body exposure, Scheduled acetaminophen, body exposure,

cooling blanketcooling blanket

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• Osmotherapy with mannitolOsmotherapy with mannitol– Decreases extracellular fluid in brainDecreases extracellular fluid in brain– Intermittent doses for ICP spikes or Intermittent doses for ICP spikes or

scheduled if elevated ICP is persistentscheduled if elevated ICP is persistent– Adverse effects:Adverse effects:

• Hypernatremia, hypokalemiaHypernatremia, hypokalemia• HyperosmolalityHyperosmolality• Hemodilution and drop in hematocritHemodilution and drop in hematocrit• Hypotension Hypotension

– Follow serum osmolality and NaFollow serum osmolality and Na• Hold mannitol if serum osm > 320 mOsm/lHold mannitol if serum osm > 320 mOsm/l

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• Drainage of CSFDrainage of CSF– Possible if ventricular catheter is in Possible if ventricular catheter is in

placeplace– CSF drainage pressure usually set at CSF drainage pressure usually set at

20 cm H20 cm H22OO

– CSF drains when ICP exceeds drainage CSF drains when ICP exceeds drainage pressurepressure

– Ventricular catheters cannot be placed Ventricular catheters cannot be placed if cerebral edema has obliterated or if cerebral edema has obliterated or significantly compressed ventriclessignificantly compressed ventricles

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• Second tier therapies for Second tier therapies for intracranial hypertension refractory intracranial hypertension refractory to sedation, muscle relaxation, to sedation, muscle relaxation, osmotherapy, and moderate osmotherapy, and moderate hypothermia:hypothermia:– barbiturate “coma”barbiturate “coma”– induced hypertensioninduced hypertension– decompressive craniotomydecompressive craniotomy– hypothermiahypothermia

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ICU MANAGEMENT OF MANAGEMENT OF

INCREASED ICPINCREASED ICP• Barbiturate “coma”Barbiturate “coma”

– ICP control is the principal endpointICP control is the principal endpoint– EEG burst suppression is a useful guide EEG burst suppression is a useful guide

to optimal barbiturate dosageto optimal barbiturate dosage• Pentobarbital 10mg/kg followed by Pentobarbital 10mg/kg followed by

infusion at 1 mg/kg/hr, titrated to effectinfusion at 1 mg/kg/hr, titrated to effect• May give additional boluses during May give additional boluses during

infusion for acute spikes in ICPinfusion for acute spikes in ICP• Moderate doses cause sluggishly reactive Moderate doses cause sluggishly reactive

pupils while large doses may cause mid pupils while large doses may cause mid position to 5 mm nonreacting pupilsposition to 5 mm nonreacting pupils

• Watch for hypotensionWatch for hypotension

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INCREASED ICPINCREASED ICP• Induced hypertensionInduced hypertension

– Inotropes to increase MAP, even beyond Inotropes to increase MAP, even beyond normal for age, to achieve an optimal CPPnormal for age, to achieve an optimal CPP• DopamineDopamine• NorepineprineNorepineprine

– Rise in ICP in tandem with a rise in MAP Rise in ICP in tandem with a rise in MAP implies total loss of autoregulation and is a implies total loss of autoregulation and is a poor prognostic signpoor prognostic sign

• Decompressive craniotomyDecompressive craniotomy– Large portion of cranium removed to allow Large portion of cranium removed to allow

room for brain to swell and minimize room for brain to swell and minimize ischemiaischemia

– Dura must be opened as wellDura must be opened as well

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INCREASED ICPINCREASED ICP• HypothermiaHypothermia

– Core body temp of 32Core body temp of 32oo to 33 to 33oo C C– Reduced cerebral metabolic activity, Reduced cerebral metabolic activity,

reducing ICPreducing ICP– Also has cytoprotective effectsAlso has cytoprotective effects– Adverse effectsAdverse effects

• ArrythmiasArrythmias• CoagulopathiesCoagulopathies• HypokalemiaHypokalemia• Increased risk of infectionIncreased risk of infection

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ICU MANAGEMENT OF OTHER MANAGEMENT OF OTHER

SYSTEMSSYSTEMS• RespiratoryRespiratory

– Maintain normocapniaMaintain normocapnia• Hyperventilation only appropriate during early Hyperventilation only appropriate during early

diagnosis and management or if herniation is diagnosis and management or if herniation is impendingimpending

– Maintain oxygenationMaintain oxygenation• pOpO2 2 > 100 is optimal> 100 is optimal

– PEEP to maintain alveolar recruitmentPEEP to maintain alveolar recruitment• ARDS, neurogenic pulmonary edema frequent ARDS, neurogenic pulmonary edema frequent

complicationscomplications• Hypoxemia has more deleterious effects on brain Hypoxemia has more deleterious effects on brain

than modest venous congestion caused by PEEPthan modest venous congestion caused by PEEP• PEEP of 5 to 10 cm HPEEP of 5 to 10 cm H22O not shown to have O not shown to have

detrimental effect on neurologic outcomedetrimental effect on neurologic outcome

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SYSTEMSSYSTEMS• CardiovascularCardiovascular

– Maintain normal blood pressureMaintain normal blood pressure• Hypotension significantly reduces CPPHypotension significantly reduces CPP• Inotropes if necessary to maintain normal Inotropes if necessary to maintain normal

BPBP– Induced hypertension if necessary Induced hypertension if necessary

• GastrointestinalGastrointestinal– Stress gastritis prophylaxis with HStress gastritis prophylaxis with H22 blocker blocker– Jejunal feeds to maintain healthy intestinal Jejunal feeds to maintain healthy intestinal

mucosa and prevent bacterial translocation mucosa and prevent bacterial translocation from gutfrom gut

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SYSTEMSSYSTEMS• Fluids, Electrolytes, NutritionFluids, Electrolytes, Nutrition

– Goal is NORMOVOLEMIAGoal is NORMOVOLEMIA• Total fluid intake should be @ 100% Total fluid intake should be @ 100%

maintenancemaintenance• Bolus as necessary to achieve normal CVPBolus as necessary to achieve normal CVP

– Avoid hypotonic fluidsAvoid hypotonic fluids• Lactated Ringer’s and 0.9% saline w/ 20 mEq Lactated Ringer’s and 0.9% saline w/ 20 mEq

KCl/l are good choices for maintenance fluidsKCl/l are good choices for maintenance fluids– Follow electrolytes closelyFollow electrolytes closely

• Avoid hyponatremiaAvoid hyponatremia• Mannitol can cause electrolyte abnormalitiesMannitol can cause electrolyte abnormalities• Watch for SIADH, diabetes insipidus, Watch for SIADH, diabetes insipidus,

cerebral salt wastingcerebral salt wasting

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SYSTEMSSYSTEMS• Fluids, electrolytes, nutritionFluids, electrolytes, nutrition

– Provide calories to meet metabolic demands of Provide calories to meet metabolic demands of patientpatient• Increased metabolic demands during acute Increased metabolic demands during acute

phase of injuryphase of injury• Heavily sedated, relaxed, cooled patient has Heavily sedated, relaxed, cooled patient has

decreased metabolic demandsdecreased metabolic demands• Enteral feedings via nasojejunal catheter Enteral feedings via nasojejunal catheter

preferable to TPN if gut deemed to be healthypreferable to TPN if gut deemed to be healthy– Avoid hyperglycemiaAvoid hyperglycemia

• Associated with poor neurologic outcomeAssociated with poor neurologic outcome• Watch serum glucose closely if dextrose Watch serum glucose closely if dextrose

containing fluids usedcontaining fluids used

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SYSTEMSSYSTEMS• RenalRenal

– Place foley for strict I’s and O’sPlace foley for strict I’s and O’s

• HematologicHematologic– Coagulopathy common with head injuriesCoagulopathy common with head injuries

• Brain derived thromboplastin activator Brain derived thromboplastin activator substances releasedsubstances released

– Follow PT/PTT or DIC screens Follow PT/PTT or DIC screens – Blood component replacement if evidence of Blood component replacement if evidence of

active bleeding or if surgical intervention active bleeding or if surgical intervention anticipatedanticipated

– Maintain normal hematocrit to optimize Maintain normal hematocrit to optimize oxygen deliveryoxygen delivery

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SYSTEMSSYSTEMS• EndocrineEndocrine

– DIABETES INSIPIDUSDIABETES INSIPIDUS• Complete or partial failure of ADH Complete or partial failure of ADH

secretion from shearing of pituitary stalksecretion from shearing of pituitary stalk• Polyuria, hypernatremia, urine osm < Polyuria, hypernatremia, urine osm <

plasma osmplasma osm• Treatment:Treatment:

Run maintenance fluids @ 100%Run maintenance fluids @ 100%Replace urine output cc for cc with Replace urine output cc for cc with dextrose-containing fluidsdextrose-containing fluidsContinuous vasopressin infusion or DDAVP Continuous vasopressin infusion or DDAVP (subQ or intranasal) q 12 to 24 hrs(subQ or intranasal) q 12 to 24 hrs

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SYSTEMSSYSTEMS• EndocrineEndocrine

– CEREBRAL SALT-WASTINGCEREBRAL SALT-WASTING• ANP-like substance released from brain, ANP-like substance released from brain,

inducing natriuresis and diuresisinducing natriuresis and diuresis

– SIADHSIADH• Elevated level of ADH inappropriate for Elevated level of ADH inappropriate for

prevailing osmotic or volume stimuliprevailing osmotic or volume stimuli• Hyponatremia, hypo-osmolality, urine Hyponatremia, hypo-osmolality, urine

osm > plasma osm, high urine Naosm > plasma osm, high urine Na• Treatment is water restrictionTreatment is water restriction

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SUMMARYSUMMARY• Identify and treat primary brain injuryIdentify and treat primary brain injury

– Rule out neurosurgical emergencyRule out neurosurgical emergency

• Minimize secondary ischemic brain injury Minimize secondary ischemic brain injury by promoting cerebral perfusionby promoting cerebral perfusion– Maintain normovolemia and adequate BPMaintain normovolemia and adequate BP– Maintain normal electrolytes and Maintain normal electrolytes and

euglycemiaeuglycemia– Maintain normocapnia and adequate Maintain normocapnia and adequate

oxygenationoxygenation– Avoid factors that increase ICPAvoid factors that increase ICP– Treat intracranial hypertensionTreat intracranial hypertension

Documents

UTHSCSA Pediatric Resident Curriculum for the PICU HEAD INJURY AND INTRACRANIAL HYPERTENSION