evidenced-based care of the child with traumatic head injury tara trimarchi msn, crnp pediatric...
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Evidenced-Based Care of the Child with Traumatic Head Injury
Tara Trimarchi MSN, CRNPPediatric Intensive Care Unit
The Children’s Hospital of PhiladelphiaUniversity of Pennsylvania
School of Nursing
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Objectives
• Discuss the scientific rationale for the therapeutic interventions used in the care of brain injured children
• Provide research based recommendations for the care of children with traumatic brain injury
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Monroe- Kellie Principle
Copied from: Rogers (1996) Textbook of Pediatric Intensive Care p. 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 blocked by 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 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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Primary mechanical injury & secondary hypoxic-ischemic injury
Neuronal Response to Injury
ATP
Glucose
Lactate
Acidosis
ONMDA
Ca+
Glutamate
Fluid
Arachidonic Acid
Leukotriene Thromboxane Prostaglandin
Edema
Cyclooxygenase Lipoxygenase
Inflammation: Vasoreactivity Thrombosis Neutrophils
T.Trimarchi 2000
.
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Is hyperglycemia detrimental?• Hyperglycemia is associated with high brain lactate levels and possibly greater
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 management
Chopp 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) Pediatric Neurosurgery, 24(6)
GCS, hypoxemia and radiologic evidence of SAH, cerebral edema and DAI are predictive of morbidity
GCS alone does not predict morbidity
Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)
Hypotension is predictive of morbidity
GCS and Pediatric Trauma Score are not predictive of outcome
Scherer & Spangenberg, (1998) Critical Care Medicine, 26(1)
Fibrinogen and platelets are significantly decreased in TBI patients
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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, development 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 Textbook www.med.ub.es/All-Net/english/neuropage/protect/vent-5htm
Originally adapted from research by Skippen et al. (1997) Critical Care Medicine, 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
--- Moderate and 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 in the 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 of edema 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 of fluid out of cell reduces edema
Brain cell
Blood vessel
Decreasing Intracranial Pressure:
T. Trimarchi, 2000
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Diuretic Therapy
Osmotic Diuretic• Mannitol (0.25-1 gm / kg) • Increases serum osmolarity• Vasoconstriction (adenosine) / less
effect if autoregulation is impaired and if CPP is < 70
• Initial increase in blood volume, BP and ICP followed by decrease
• Questionable mechanism of lowering ICP – Rosner et al. (1987)
Neurosurgery, 21(2)
Loop Diuretic• Furosemide• Decreased CSF formation• Decreased systemic and
cerebral blood volume (impairs sodium and water movement across blood brain barrier)
• May have best affect in conjunction with mannitol
– Pollay et al. (1983) Journal of Neurosurgery, 59 ; Wilkinson (1983) Neurosurgery,12(4)
Decreasing Intracranial Pressure:
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Hypertonic Fluid Administration
• Fisher et al. (1992) Journal of Neurosurgical Anesthesiology, 4– Reduction 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 continuous infusion of 3%
sadium acetate solution– Little continued benefit after 72 hours of treatment
Decreasing Intracranial Pressure:
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Copied from: Qureshi et al. (1998) Critical Care Medicine, 26(3)
Goal:
Sodium 145-155 mmol/L
Hyperosmolar Therapy
• Sodium: square
• ICP: circle
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Decrease Intracranial Pressure: Promote Venous DrainageKeep neck mid-line and elevate head of bed …. To what degree?
Image from: Dicarlo in ALL-NET Pediatric Critical Care Textbook www.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 Neuroscience Nursing, 22(6)
Parsons & Wilson (1984) Nursing Research, 33(2)
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Management of Pain & Agitation• Opiods• Benzodiazepines
Management of Movement• Neuromuscular blockade may be required - use only when necessary
Problems:
• Difficult to assess neurologic exam
• Risk of hypotension
Use short acting 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 been documented with use of opiods. But, elevation in ICP is transient and there is no resulting ischemia from decreased MAP / CPP.
Albanese et al. (1999) Critical Care Medicine, 27(2)
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0
2
4
6
8
10
12
14
16
18
20
Before During After
TurningSuctioningBathing
Nursing Activities and ICP
Rising (1993) Journal of Neuroscience Nursing, 25(5)
ICP
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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
HyperventIV lidoIT lido
53%
0%
Percent increase in ICP with suctioning using preemptive hyperventilation, IV lidocaine and IT lidocaine
Wainright & Gould (1996)Individualize suctioning practices according the patient’s response
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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 and preparation before spending time at bedside !
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Reduction of Cerebral Metabolic Rate
• Goal: Reduce cerebral oxygen requirement
– Anticonvulsants • To prevent seizure activity
– Pentobarbital ??• Adverse effects include hypotension and bone marrow
dysfunction• Used only after unsuccessful attempts to control ICP and
maximize CPP with other therapies• Improved outcome not fully supported by research
Traeger et al. (1983) Critical Care Medicine, 11
Ward et al. (1985) Journal of Neurosurgery, 62(3)
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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) by 45% 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 C have good outcomes vs. 38% of patients in control group
Side-effects:• Potassium flux• Coagulopathy• Shivering• Skin Breakdown
Requires:
• Slow re-warming• Close monitoring
No pediatric studies!
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Summary of Recommended Practices
• 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 patient response)
– Normoventilate
– Support circulation / maximize cerebral perfusion pressure
– Maintain mean arterial blood pressure and maintain CPP (goal > 60)
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Summary of Recommended Practices
• 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 supports elevation not > 30
degrees)– Treat pain and agitation - consider pre-medication for nursing activities, +/-
neuromuscular blockade (only when needed)– Careful monitoring of ICP during nursing care, cluster nursing activities and limit
handling when possible– Suction only as needed, limit passes, pre-oxygenate / +/- pre-hyperventilate (PaCo2
not < 30) / use lidocaine IV or IT when possible– After careful preparation of visitors, allow calm contact
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Summary of Recommended Practices
• Decrease Cerebral Metabolic Rate
– Prevent seizures
– Reserve pentobarbital for refractory conditions
– Avoid hyperthermia, +/- hypothermia
– Avoid hyperglycemia (early)