Evidenced-Based Care of the Child with Traumatic Head

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 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 • 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 Pa. Co 2 (mm. Hg) Normal 60 - 150 mm. Hg Normal 30 - 50 mm. Hg 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 (SJVO 2) • Arteriojugular Venous Oxygen Difference (AJVO 2) • Cerebral Metabolic Rate For Oxygen (CMRO 2) Possible better outcome when used (adult study) Cruz (1998) Critical Care Medicine, 26(2) • Brain Sensors • Brain tissue p. H, Pa. O 2, Pc. O 2, 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 H 2 O 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-5 htm

Research Supporting Normoventilation • Forbes et al. (1998) Journal of Neurosurgery, 88(3) • Marion et al. (1995) New Horizons, 3(3) • Mc. Laughlin & 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 cm. H 20 --- Moderate and transient ---

Circulatory Support: Maintain Cerebral Perfusion Pressure CPP = MAP - ICP 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 mm. Hg) 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 Problems: • Opiods • Benzodiazepines • Difficult to assess neurologic exam Management of Movement • Risk of hypotension • Neuromuscular blockade may be required - use only when necessary 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 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% 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 otherapies • 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 (CMRO 2) 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 (Pa. Co 2 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)