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

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

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

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

• 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

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

.

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

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

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 ???

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

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

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

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

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

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

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

Decreasing Intracranial Pressure:

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

Goal:

Sodium 145-155 mmol/L

Hyperosmolar Therapy

• Sodium: square

• ICP: circle

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)

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)

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

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

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 !

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 / +/- pre-hyperventilate (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)