head trauma research

8/11/2019 Head Trauma Research

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Evidenced-Based

Care of the Childwith Traumatic HeadInjury

Tara Trimarchi MSN, CRNP

Pediatric Intensive Care Unit

The Childrens Hospital of Philadelphia

University of Pennsylvania

School of Nursing


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Objectives

Discuss the scientific rationalefor the therapeutic

interventions used in the care of brain injuredchildren

Provide research based recommendationsfor the care

of children with traumatic brain injury


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Monroe- Kellie Principle

Copied from: Rogers (1996) Textbook of Pediatric Intensive Carep. 646


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Traumatic Mass Occupying Lesions

Epidural hematoma

Subdural hematoma

Subarachnoid hemorrhage

Intra-paranchymal hemorrhage


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Cerebral Spinal Fluid

Produced by the choroid plexus

Average volume 90 - 150 ml

(0.35 ml / minute or 500 ml / day)

Reabsorbed through the arachnoid villi

Drainage may be blockedby inflammation of the

arachnoid villi, diffuse cerebral edema, mass effect of

hemorrhage or intraventricular hemorrhage


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CBF

MAP(mmHg)

Normal

50 - 100

ml / min

Normal 60 - 150 mmHg

Cerebral Blood Flow

Regulation of Cerebral Vascular Resistance

PaCo2(mmHg)

Normal 30 - 50 mmHg

Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care

pp. 648 - 651


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Cerebral Edema

Cellular response to injury

Primary injury (mechanical trauma at time of event) and ...

Secondary injury

Hypoxic-ischemic injury

Injured neurons have increased metabolic needs

Concurrent hypotension and hypoxemia may be

present

Inflammatory response results


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Shearing injury of axons

Deep cerebral cortex, thalamus, basal gangliaPunctate hemorrhage and diffuse cerebral edema

Image from: Neuroscience for Kidswww.faculty.washington.edu/chudler/cells/html

Diffuse Axonal Injury


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Primary mechanical injury & secondary hypoxic-ischemic injury

Neuronal Response to Injury

ATP

Glucose

Lactate

Acidosis

ONMDA

Ca+

Glutamate

Fluid

Arachidonic AcidLeukotrieneThromboxaneProstaglandin

Edema

Cyclooxygenase

Lipoxygenase

Inflammation:VasoreactivityThrombosisNeutrophils

T.Trimarchi 2

.


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Is hyperglycemia detrimental?

Hyperglycemia is associated with high brain lactate levels and possiblygreater cerebral cellular injury, particularly in the early phases of brain

injury (animal research / not conclusive / older studies)Recommendation: Avoid hyperglycemia, particularly during the

early stages of brain injury. Consider the use of intravenous

solutions that do not contain dextrose for early fluid and electrolyte

managementChopp et al., (1988). Stroke, 19.

Lanier et al., (1987). Anesthesiology, 66.

Ljunggren et al. (1974). Brain Research, 77.

Myers et al., (1976). Journal of Neuropathology and Experiemental Neurology, 35

Smith et al. (1986). Journal of Cerebral Blood Flow and Metabolism, 6.Natale et al. (1990). Resuscitation, 19.

Source:Rogers (1996) Textbook of Pediatric Intensive Care pp.702-704


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Monitoring Brain Metabolism

Jugular Venous Catheter

Jugular Venous Oxygen Saturation (SJVO2)

Arteriojugular Venous Oxygen Difference (AJVO2)

Cerebral Metabolic Rate For Oxygen (CMRO2)

Possible better outcome when used (adult study)

Cruz (1998) Critical Care Medicine, 26(2)

Brain Sensors

Brain tissue pH, PaO2, PcO2, lactate

Kiening (1997) Neurology Research, 19(3)


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Basic Monitoring

Serial neurologic examinations

Circulation / respiration Intracranial Pressure

Cerebral Perfusion Pressure

Radiologic Studies

Laboratory Studies

Ong et al. (1996) PediatricNeurosurgery, 24(6)

GCS, hypoxemia and

radiologic evidence of SAH,cerebral edema and DAI arepredictive of morbidity

GCS alone does not predictmorbidity

Kokoska et al. (1998), Journalof Pediatric Surgery, 33(2)

Hypotension is predictive ofmorbidity

GCS and Pediatric TraumaScore are not predictive ofoutcome

Scherer & Spangenberg,(1998) Critical CareMedicine, 26(1)

Fibrinogen andplatelets aresignificantlydecreased in TBIpatients


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Overview:Management of Traumatic Head Injury

Maximize oxygenation and ventilation

Support circulation / maximize cerebral perfusion

pressure

Decrease intracranial pressure

Decrease cerebral metabolic rate


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Respiratory Support: Maximize Oxygenation

Hypoxemia is predictive of morbidity

Ong et al. (1996) Pediatric Neurosurgery, 24(6) Neurogenic pulmonary edema, concurrent lung injury, developmen

of ARDS may be present

Is use of Positive End Expiratory Pressure to maximize

oxygenation a safe practice?

May impair cerebral venous return

Cooper et al. (1985) Journal of Neurosurgery, 63

PEEP > 10 cm H2O increases ICP

Feldman et al. (1997) Journal of Neurosurgical

Anesthesiology, 9(2)


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Respiratory Support: Normoventilation

Hyperventilation : Historical management more harm than good ???

Image from: ALL-NET Pediatric Critical Care Textbookwww.med.ub.es/All-Net/english/neuropage/protect/vent-5htm

Originally

adapted from

research by

Skippen et al(1997) Critic

Care Medicin

25

CBF pre- hyperventilation CBF post-hyperventilation


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Research Supporting Normoventilation

Forbes et al. (1998) Journal of Neurosurgery, 88(3)

Marion et al. (1995) New Horizons, 3(3)

McLaughlin & Marion (1996) Journal of Neurosurgery, 85(5)

Muizelaar et al. (1991) Journal of Neurosurgery, 75(5)

Newell et al. (1996) Neurosurgery, 39(1)

Skippen et al. (1997) Critical Care Medicine, 25(8)

Yundt & Diringer (1997) Critical Care Clinics, 13(1)


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Use of Hyperventilation ...

Transient management of very acute and serious elevation of

intracranial pressure

Possible role for occassional, preemptive use before activities

known to seriously increase intracranial pressure

No lower than 32-35 cmH20

--- Moderateand transient---


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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 inthe first 24

hours after

TBI

Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)

CPP = MAP - ICP


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Circulatory Support:

Maintain Cerebral Perfusion Pressure

Adelson et al. (1997) Pediatric Neurosurgery, 26(4)

Children (particularly < 24 months old) are at increased

risk of cerebral hypo-perfusion after TBI

Low CBF is predictive of morbidity

Rosner et al. (1995) Journal of Neurosurgery, 83(6)

Management aimed at maintaining CPP (70 mmHg)improves outcomes

CPP = MAP - ICP


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Decreasing Intracranial

Pressure

Evacuate hematoma

Drain CSF

Intraventricular catheters use is limited by degree ofedema and ventricular effacement

Craniotomy

Permanence, risk of infection, questionable benefit

Reduce cerebral edema

Promote venous return

Reduce activity associated with elevated ICP

Reduce cerebral metabolic rate

Brain Blood

CSF MassBone


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Hyperosmolar Therapy: Increase Blood Osmolarity

Fluid

Osmosis: Fluid will move from area of lower osmolarity to an

area of higher osmolarity

Movement offluid out of cellreduces edema

Braincell

Bloodvessel

Decreasing Intracranial Pressure:

T. Trimarchi, 200

D i I i l P


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Diuretic Therapy

Osmotic Diuretic

Mannitol (0.25-1 gm / kg)

Increases serum osmolarity

Vasoconstriction (adenosine) /less effect if autoregulation isimpaired and if CPP is < 70

Initial increase in bloodvolume, BP and ICP followed

by decrease

Questionable mechanism of

lowering ICPRosner et al. (1987)

Neurosurgery, 21(2)

Loop Diuretic

Furosemide Decreased CSF formation

Decreased systemic andcerebral blood volume(impairs sodium and water

movement across blood brainbarrier)

May have best affect inconjunction with mannitol

Pollay et al. (1983)Journal of Neurosurgery,

59 ; Wilkinson (1983)

Neurosurgery,12(4)



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Hypertonic Fluid Administration

Fisher et al. (1992) Journal of Neurosurgical Anesthesiology, 4Reduction in mean ICP in children 2 hours after bolus

administration of 3% saline

Taylor et al. (1996) Journal of Pediatric Surgery,31(1)

ICP is lowered by resuscitation with hypertonic saline vs.lactated ringers solution in an animal model

Qureshi et al. (1998) Critical Care Medicine, 26(3)

Reduction in mean ICP within 12 hours of continuousinfusion of 3% sadium acetate solution

Little continued benefit after 72 hours of treatment



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D I i l P P V D i


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Decrease Intracranial Pressure: Promote Venous Drainage

Keep neck mid-line and elevate head of bed . To what degree?

Image from: Dicarlo in ALL-NET Pediatric Critical Care Textbookwww.med.ub.es/All-Net/english/neuropage/protect/icp-tx-3.htm

Feldman et al.(1992) Journal of

Neurosurgery, 76

March et al.(1990) Journal of

NeuroscienceNursing, 22(6)

Parsons & Wilson(1984) NursingResearch, 33(2)

D I t i l P


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Management of Pain & Agitation

Opiods Benzodiazepines

Management of Movement

Neuromuscular blockade may berequired - use only when necessary

Problems:

Difficult to

assess neurologicexam

Risk ofhypotension

Use shortacting agents

Decrease Intracranial Pressure:

Do opiods increase CBF and ICP as well as lower MAP and CPP?

Increased ICP with concurrent decreased MAP and CPP has beendocumented with use of opiods. But, elevation in ICP is transient andthere is no resulting ischemia from decreased MAP / CPP.

Albanese et al. (1999) Critical Care Medicine, 27(2)


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0

2

4

68

10

12

14

1618

20

Before During After

Turning

Suctioning

Bathing

Nursing Activities and ICP

Rising (1993) Journal of Neuroscience Nursing, 25(5)

ICP

Suctioning Practices


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Suctioning Practices

Hyper-oxygenation

Mild / moderate hyperventilation

Brown & Peeples (1992) Heart &Lung, 21

Parsons & Shogan (1982) Heart &Lung, 13

Intratracheal / intravenous lidocaine

Donegan & Bedford (1980)Anesthesiology, 52

Wainright & Gould (1996)Intensive & Critical Care Nursing,12

Hypervent

IV lido

IT lido

53%

0%

Percentincrease

ICP with

suctioning using

preemptive

hyperventilation

IV lidocaine and

lidocaine

Wainright & Gould (1996)Individualize suctioning practicesaccording the patients response

F il C d ICP


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Family Contact and ICP

Bruya (1981) Journal of Neuroscience Nursing, 13

Hendrickson (1987) Journal of Neuroscience Nursing,19(1)

Mitchell (1985) Nursing Administration Quarterly, 9(4)

Treolar (1991) Journal of Neuroscience Nursing, 23(5)

Presence, touch and voice of family / significant others...

Does not significantly increase ICP

Has been demonstrated to decrease ICP

Note: Visitors require education andpreparation before spending time at bedside !


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Reduction of Cerebral Metabolic Rate: Hypothermia

Metz et al. (1996) Journal of Neurosurgery, 85(4)

32.5 C reduced cerebral metabolic rate for oxygen (CMRO2) by45% without change in CBF

intracranial pressure decreased significantly (p < 0.01)

Marion et al. (1997) New England Journal of Medicine, 336(8)

At 12 months, 62% of patients (GCS of 5-7) cooled to 32-33 Chave good outcomes vs. 38% of patients in control group

Side-effects:

Potassium flux

CoagulopathyShivering

Skin Breakdown

Requires:

Slow re-warming

Close monitoring

No

pediatricstudies!

Summary of Recommended Practices


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Serial neurologic assessments and physical examination

Continuous cardio-respiratory, ICP, and CPP monitoring, +/-cerebral metabolism monitoring adjuncts

Maximize Oxygenation and Ventilation

Maximize oxygenation (cautious use of PEEP / keep PEEP < 10 to

prevent inhibited venous return / individualize according to patientresponse)

Normoventilate

Support circulation / maximize cerebral perfusion pressure

Maintain mean arterial blood pressure and maintain CPP (goal > 60)



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Decrease intracranial pressure

Evacuate mass occupying hemorrhages

Consider draining CSF with ventriculostomy when possible Hyperosmolar therapy, +/- diuresis (cautious use to avoid

hypovolemia and decreased BP)

Mid-line neck, elevated head of bead (some research supportselevation not > 30 degrees)

Treat pain and agitation - consider pre-medication for nursingactivities, +/- neuromuscular blockade (only when needed)

Careful monitoring of ICP during nursing care, cluster nursingactivities and limit handling when possible

Suction only as needed, limit passes, pre-oxygenate / +/- pre-

hyperventilate (PaCo2 not < 30) / use lidocaine IV or IT whenpossible

After careful preparation of visitors, allow calm contact



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Decrease Cerebral Metabolic Rate

Prevent seizures

Reserve pentobarbital for refractory conditions

Avoid hyperthermia, +/- hypothermia

Avoid hyperglycemia (early)

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