Evidenced-Based Care of the Child with Traumatic Head Injury

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Transcript Evidenced-Based Care of the Child with Traumatic Head Injury

Evidenced-Based
Care of the Child
with Traumatic Head
Injury
Tara Trimarchi MSN, CRNP
Pediatric Intensive Care Unit
The Children’s Hospital of Philadelphia
University of Pennsylvania
School of Nursing
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
Monroe- Kellie Principle
Copied from: Rogers (1996) Textbook of Pediatric Intensive Care
p. 646
Traumatic Mass Occupying Lesions
• Epidural hematoma
• Subdural hematoma
• Subarachnoid hemorrhage
• Intra-paranchymal hemorrhage
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
Cerebral Blood Flow
Regulation of Cerebral Vascular Resistance
CBF
Normal
50 - 100
ml / min
MAP
PaCo2
(mmHg)
(mmHg)
Normal 60 - 150 mmHg
Normal 30 - 50 mmHg
Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care
pp. 648 - 651
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
Diffuse Axonal Injury
• 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
Neuronal Response to Injury
Primary mechanical injury & secondary hypoxic-ischemic injury
O
Ca+
Lactate
ATP
Glucose
Acidosis
Inflammation:
Vasoreactivity
Thrombosis
Neutrophils
NMDA
.
Edema
Glutamate
Cyclooxygenase
Lipoxygenase
Arachidonic Acid
Leukotriene
Thromboxane
Prostaglandin
Fluid
T.Trimarchi 2000
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
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)
Basic Monitoring
•
•
•
•
•
•
Serial neurologic examinations
Circulation / respiration
Intracranial Pressure
Cerebral Perfusion Pressure
Radiologic Studies
Laboratory Studies
Scherer & Spangenberg,
(1998) Critical Care
Medicine, 26(1)
Fibrinogen and
platelets are
significantly
decreased in TBI
patients
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
Overview:
Management of Traumatic Head Injury
• Maximize oxygenation and ventilation
• Support circulation / maximize cerebral perfusion
pressure
• Decrease intracranial pressure
• Decrease cerebral metabolic rate
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)
Respiratory Support: Normoventilation
Hyperventilation : Historical management more harm than good ???
CBF pre- hyperventilation CBF post-hyperventilation
Originally
adapted from
research by
Skippen et al.
(1997) Critical
Care Medicine,
25
Image from: ALL-NET Pediatric Critical Care Textbook
www.med.ub.es/All-Net/english/neuropage/protect/vent-5htm
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)
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 ---
Circulatory Support:
Maintain Cerebral Perfusion Pressure
CPP = MAP - ICP
6
5
Number of
4
Hypotensive
Episodes in 3
the first 24
hours after 2
TBI
Good
Moderate
Severe
Vegetative
Dead
1
0
Patient Outcome
Kokoska et al. (1998), Journal of Pediatric Surgery, 33(2)
CPP = MAP - ICP
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
Decreasing Intracranial
Pressure
Brain
Blood
CSF
Mass
• Evacuate hematoma
Bone
• 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
Decreasing Intracranial Pressure:
Hyperosmolar Therapy: Increase Blood Osmolarity
Brain
cell
Fluid
Blood
vessel
Movement of
fluid out of cell
reduces edema
Osmosis: Fluid will move from area of lower osmolarity to an
area of higher osmolarity
T. Trimarchi, 2000
Decreasing Intracranial Pressure:
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:
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
Hyperosmolar Therapy
Goal:
Sodium 145-155
mmol/L
• Sodium: square
• ICP: circle
Copied from: Qureshi et al. (1998) Critical Care Medicine, 26(3)
Decrease Intracranial Pressure: Promote Venous Drainage
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)
Image from: Dicarlo in ALL-NET Pediatric Critical Care Textbook
www.med.ub.es/All-Net/english/neuropage/protect/icp-tx-3.htm
Decrease Intracranial Pressure:
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
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)
Nursing Activities and ICP
20
18
16
14
ICP
12
Turning
Suctioning
Bathing
10
8
6
4
2
0
Before
During
After
Rising (1993) Journal of Neuroscience Nursing, 25(5)
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
Individualize suctioning practices
according the patient’s response
53%
Percent increase in
ICP with
suctioning using
preemptive
hyperventilation,
IV lidocaine and IT
lidocaine
0%
Hypervent
IV lido
IT lido
Wainright & Gould (1996)
Family Contact and ICP
Presence, touch and voice of family / significant others...
•
Does not significantly increase ICP
•
Has been demonstrated to decrease 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)
Note: Visitors require education and
preparation before spending time at bedside !
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)
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!
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)
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 / +/- prehyperventilate (PaCo2 not < 30) / use lidocaine IV or IT when
possible
– After careful preparation of visitors, allow calm contact
Summary of Recommended Practices
• Decrease Cerebral Metabolic Rate
– Prevent seizures
– Reserve pentobarbital for refractory conditions
– Avoid hyperthermia, +/- hypothermia
– Avoid hyperglycemia (early)