evidenced-based care of the child with traumatic head injury

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Evidenced-Based Care of the Child with Traumatic Head Injury A. Student The Children’s Hospital of Philadelphia Dr. Abdul-Monim Batiha Dr. Abdul-Monim Batiha

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Evidenced-Based Care of the Child with Traumatic Head Injury. A. Student The Children’s Hospital of Philadelphia Dr. Abdul-Monim Batiha. Objectives. Describe the pathophysiology of traumatic brain injury - PowerPoint PPT Presentation

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Evidenced-Based Care of the Child with Traumatic Head Injury

A. StudentThe Children’s Hospital of Philadelphia

Dr. Abdul-Monim BatihaDr. Abdul-Monim Batiha

Objectives

• Describe the pathophysiology of traumatic brain injury

• 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

Rhoads & Pflanzer (1996) Human Physiology p. 211

Traumatic Head Injury

ALL-NET Pediatric Critical Care Textbook Source: LifeART EM Pro (1998) Lippincott Williams & Wilkins. www.med.ub.es/All-Net/english/neuropage/trauma/head-8htm

Layers of the Cranial Vault

Anatomy of the Brain www.neurosurgery.org/pubpgages/patres/anatofbrain.html#micro

Epidural and Subdural Hematoma

ALL-NET Pediatric Critical Care Textbook - Source: LifeART EM Pro (1998) Lippincott Williams & Wilkins. www.med.ub.es/All-Net/english/neuropage/trauma/head-8htm

Subarachnoid Hemorrhage

Rogers (1996) Textbook of Pediatric Intensive Care pp. 829

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

Brain Cells

Rhoads & Pflanzer (1996) Human Physiology p. 213

Concussion

Contusion

Intracerebral hemorrhage

Neurons

Diffuse Axonal Injury• Shearing injury of axons

Deep cerebral cortex, thalamus, basal ganglia• Punctate hemorrhage and paranchymal edema

Neuroscience for Kids www.faculty.washington.edu/chudler/cells/html

CBF

MAP(mmHg)

Normal 50 - 100 ml / min

Normal 60 - 150 mmHg

Cerebral Blood FlowRegulation of Cerebral Vascular Resistance

PaCo2 (mmHg)

Normal 30 - 50 mmHg

Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651

Cerebral Edema

• Cellular response to injury

– Primary injury

• Secondary injury

– Hypoxic-ischemic injury

• Injured neurons have increased metabolic needs

• Concurrent hypotension and hypoxemia

• Inflammatory response

Primary mechanical injury & secondary hypoxic-ischemic injury

Neuronal Response to Injury

ATP

Glucose

Lactate

Acidosis

O2 -NMDA

Ca+

Glutamate

Fluid

Arachidonic Acid

Leukotriene Thromboxane Prostaglandin

Edema

Cyclooxygenase Lipoxygenase

Inflammation: Vasoreactivity Thrombosis Neutrophils

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 in adults

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

Brain Sensors

Brain tissue pH, PaO2, PcO2, lactate

Kiening (1997) Neurology Research, 19(3)

Cerebral Edema after Head Trauma

ALL-NET Pediatric Critical Care Textbook Source: Research by Samuel Neff MD. www.med.ub.es/All-Net/english/neuropage/trauma/head-10htm

Monroe- Kellie Principle

Rogers (1996) Textbook of Pediatric Intensive Care p. 646

Management of Traumatic Head Injury

• Maximize oxygenation and ventilation

• Support circulation / maximize cerebral perfusion

pressure

• Decrease intracranial pressure

• Decrease cerebral metabolic rate

Monitoring

• Serial neurologic examinations

• Circulation / Respiration

• Intracranial Pressure

• Radiologic Studies

• Laboratory Studies

Ong et al. (1996) Pediatric Neurosurgery, 24(6)

GCS, hypoxemia and radiologic evidence of SAH, edema and DAI predict morbidity

GCS alone does not predict morbidity

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

Hypotension is predictive of morbidity

GCS and PTS are not predictive of outcome

Scherer & Spangenberg (1998) Critical Care Medicine, 26(1)

Fibrinogen and platelets are significantly decreased in TBI patients

Respiratory Support: Maximize Oxygenation

• Hypoxemia is predictive of morbidity

– Ong et al. (1996) Pediatric Neurosurgery, 24(6)

• Neurogenic pulmonary edema / concurrent lung injury

– Positive End Expiratory Pressure

• May impair cerebral venous return– Cooper et al. (1985) Journal of Neurosurgery, 63

– Feldman et al. (1997) Journal of Neurosurgical Anesthesiology, 9(2)

• PEEP > 10 cm H2O increases ICP

Respiratory Support: NormoventilationHyperventilation : Historical management more harm than good?

ALL-NET Pediatric Critical Care Textbook www.med.ub.es/All-Net/english/neuropage/\protect/vent-5htm

Originally adapted from Skippen et al. (1997) Critical Care Medicine, 25

Evidence 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 ...

• Management of very acute elevation of intracranial pressure

• Preemptive for activities known to increase intracranial

pressure

• No lower than 32-35 cmH20

--- Moderate and transient

Suctioning

• Hyper-oxygenation• Mild / moderate hyperventilation

Brown & Peeples (1992) Heart & Lung, 21Parsons & Shogan (1982) Heart & Lung, 13

• Intratracheal / intravenous lidocaineDonegan & Bedford (1980) Anesthesiology, 52Wainright & Gould (1996) Intensive & Critical Care Nursing, 12

• As needed basis and individualize according to patient response

HyperventIV lidoIT lido

53%

0%

Percent increase in ICP with suctioning

Wainright & Gould (1996)

Circulatory Support: Maintain Cerebral Perfusion Pressure

0

1

2

3

4

5

6

Outcome

Good

Moderate

Severe

Vegetative

Dead

Number of Hypotensive Episodes

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

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 hypoperfusion 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

Lowering ICP

• Evacuate hematoma• Drain CSF

– Intraventricular catheters use is limited by degree of edema and ventricular effacement

• Craniotomy– Permanence, risk of infection, questionable benefit

• Reduce edema• Promote venous return• Reduce cerebral metabolic rate• Reduce activity associated with elevated ICP

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

Diuretic Therapy

Osmotic Diuretic• Mannitol (0.25-1 gm / kg) • Increases 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)

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%

saline acetate solution– Little continued benefit after 72 hours of treatment

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

Goal: Sodium 145-155

Hyperosmolar Therapy

Sodium: square

ICP: circle

Promote Venous DrainageKeep neck mid-line and elevate head of bed …. To what degree?

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)

Reduction of Cerebral Metabolic Rate

• Reduction in cerebral oxygen requirement

– Anticonvulsants - 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, 11Ward 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, and 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 fluxCoagulopathyShiveringSkin Breakdown

Slow re-warming

Close monitoring

No pediatric studies!

Management of Pain & Agitation• Opiods

• Benzodiazepines

Management of Movement

• Neuromuscular blockade

Difficult to assess neurologic exam

Monitor for hypotension

Short acting agents beneficial

ICP management continued...

Do opiods increase CBF?

Increased ICP with concurrent decreased MAP and CPP has been documented. 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

0

2

4

6

8

10

12

14

16

18

20

Before During After

SuctioningTurning

Nursing Activities and ICP

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

ICP

Bathing

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

Summary of Recommended Practices

• Maximize oxygenation (PEEP < 10)

• Normoventilate

• Suction only as needed, limit passes, pre-oxygenate, +/- pre-hyperventilate (not < 30), use lidocaine when possible

• Maintain blood pressure and maintain CPP > 60

• Evacuate intracranial blood

• Drain CSF with ventriculostomy when possible

Summary of Recommended Practices

• Hyperosmolar therapy

• Avoid hyperthermia, +/- hypothermia

• Prevent seizures

• Reserve pentobarbital for refractory conditions

• Mid-line neck, elevated head of bead, ? not > 30 degrees

• Treat pain and agitation - consider pre-medication for nursing activities

• Avoid hyperglycemia

• Allow family contact