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Traumatic Brain Injury. Katie Clement, MD PICU Resident Lectures 2011. Objectives. Understand the mechanisms of Pediatric Traumatic Brain Injury Understand the pathophysiology of TBI Understand the management of TBI. Overview. Epidemiology . Injury is leading cause of death for children

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Traumatic Brain Injury


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    1. Traumatic Brain Injury Katie Clement, MD PICU Resident Lectures 2011

    2. Objectives • Understand the mechanisms of Pediatric Traumatic Brain Injury • Understand the pathophysiology of TBI • Understand the management of TBI

    3. Overview

    4. Epidemiology • Injury is leading cause of death for children • 40% of those are from TBI • Mortality between 17 – 33% • Most common cause of death & disability in childhood in developed countries • 3000 children die each year from TBI in the US Krug EG et al. Am J Public Health. 2000. Langlois JA et al. Centers for Disease Control & Prevention. 2006. White JR et al. CCM. 2001. Krug EG et al. Langlois JA et al.

    5. GCS • Severity of TBI is defined by the GCS Score • Mild • GCS 13-15 • Moderate • GCS 9-12 • Severe • GCS <9

    6. GCS Total score ranges from 3 - 15

    7. Pathophysiology

    8. Effects of Trauma • Increase in volume of any or all intracranial components • Uncoupling of cerebral blood flow & metabolic activity (loss of autoregulation) can lead to excessive CBF • Increased CSF production in response to increased CBF • Hypercapnia or hypoxia (cause vasodilation & increased CBF) • Herniation, brain swelling, subarachnoid hemorrhage may obstruct flow of CSF • Hematomas, contusions, edema may increase intracranial volume

    9. Definition of ICP • ICP = ICP vascular + ICP CSF • Used to estimate cerebral perfusion pressure • CPP = MAP – mean ICP • CPP: Cerebral Perfusion Pressure • ICP: Intracranial Pressure • MAP: Mean Arterial blood Pressure

    10. Normal Values • ICP is typically ≤ 15 mmHg in adults and lower in children & newborns • ICP ≥ 20 mmHg is pathologic in adults • Physiologic events such as sneezing, coughing, Valsalva will transiently raise ICP as well • CPP normals for adults range from 50 – 70 mmHg • Not well established in children, likely 40 – 60 mmHg depending on age • When CPP falls below a critical level, brain receives inadequate blood flow

    11. Intracranial Pressure • The intracranial compartment has a fixed internal volume • Brain parenchyma – 80% • CSF – 10% • Blood – 10% • ICP is a function of the volume & compliance of each component • The Monroe-Kellie Doctrine

    12. Monroe-Kellie Principle Intracranial compensation for an expanding mass lesion Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC (Ed), Williams and Wilkins 1996. p. 646; figure 18.1.

    13. The relationship between intracranial volume and pressure is nonlinear An initial increase in volume results in a small increase in pressure because of intracranial compensation (blue line). Once intracranial compensation is exhausted, additional increases in intracranial volume result in a dramatic rise in intracranial pressure (red line).

    14. Cerebral Edema • Diffuse swelling more common among infants and children compared to adults • Infant skull is more compliant, tolerates significant deformation without fracture • Brain atrophy begins in young adulthood and allows for more room in the adult skull for brain to expand Lang DA. J Neurosurg 1994 Coats B. J Neurotrauma 2006 Kochanek PM. Dev Neurosci 2006

    15. Cerebral Edema • Worsened with hypoxia & hypoperfusion • Types of edema: • Vasogenic- breakdown of the blood-brain barrier • Cytotoxic- cellular swelling • Interstitial- periventricular exudation of cerebrospinal fluid through the ependymal lining • Osmotic- movement of water into the interstitial spaces induced by osmotically active products of tissue injury and blood clot

    16. Cerebral Autoregulation • Often impaired in children with TBI • Impaired autoregulation is associated with worse outcome Cerebral autoregulation in hypertension Kaplan, NM, Lancet 1994

    17. 2 Insults • Primary Injury • Direct injury to brain parenchyma • Blunt force: Contusions, hematomas • Acceleration-deceleration: physical shearing or tearing of axons http://www.tbilawyers.com/diffuse-axonal-injury.html

    18. Secondary Injury: • Potentially avoidable or treatable • Hypoxemia • Hypotension • Elevated ICP • Hypercarbia • Hyper- & Hypoglycemia • Electrolyte abnormalities • Enlarging hematomas • Coagulopathy • Seizures • Hyperthermia • Endogenous cascade of cellular & biochemical events • Occurs within minutes and continues for months after initial injury • Leads to neuronal cell death

    19. Diffuse Axonal Injury • Widespread damage to axons in the white matter • Corpus callosum • Basal ganglia • Periventricular white matter • Caused by • Hypoxic-ischemic injury • Calcium & ion flux • Mitochondrial & cytoskeletal dysfunction • A major cause of morbidity in pediatric TBI • More extensive DAI associated with worse outcome

    20. Evaluation

    21. Initial Evaluation • Don’t forget standard trauma protocols: • Primary Survey • ABCs! • Secondary Survey

    22. History • Mechanism of injury • Loss of consciousness + duration • Vomiting • Headache • One of the earliest symptoms of increased ICP • Progression of symptoms

    23. Physical Exam—General • Hypoxia & hypotension should be immediately identified and treated • Respiratory depression, bradycardia, and/or hypertension may indicate impending herniation and also requires prompt treatment • Maintain C-spine immobilization

    24. Neuro exam • Assign a GCS • Level of consciousness • Pupils • Extraocular movements • Funduscopic exam • Brainstem reflexes • DTRs • Response to pain

    25. Battle Sign

    26. Raccoon Eyes

    27. CSF Rhinorrhea

    28. Setting-Sun Sign • Late sign of increased intracranial pressure • Pressure on cranial nerves III, IV, and VI forces the eyes downward, revealing a rim of sclera above the irises.

    29. Funduscopic Exam www.dontshake.org http://cloud.med.nyu.edu/modules/pub/neurosurgery/cranials.html

    30. Types of Herniation • Subfalcine : uneven, one-sided expansion of a cerebral hemisphere that pushes a portion of the brain tissue (cingulate gyrus) under the falx cerebri • Uncal: medial temporal lobe is pushed against the tentorium. Can compress brainstem in severe cases • Central transtentoral : downward pressure centrally, can cause bilateral uncal herniation. • Extracranial : brain tissue pushes through an opening in the cranial cavity either surgically or by trauma • Tonsillar : swelling or bleeding in the cerebellum pushes the cerebellar tonsils downward into the foramen magnum. Life threatening b/c can compress the brainstem

    31. Signs of herniation • Uncal herniation: • Third cranial nerve palsy • Hemiplegia • Progressive changes in respiratory pattern, pupil size, vestibuloocular reflexes, posturing • Cushing’s Triad • Hypertension • Bradycardia • Slow, irregular respirations OCCURS LATE!!

    32. Mydriasis • Can be associated with CN III injury • Uncal herniation can cause unilateral mydriasis & ptosis

    33. Labs • Depends on type & extent of injury • Minimum: hct, T&S, UA • Useful in TBI: • Glucose • Hyperglycemia is a poor prognostic indicator • Electrolytes w/ osmolarity • Coags • DIC is associated with poor outcomes Chiaretti A. Childs Nerv Syst 2002.

    34. Imaging • CT is preferred initial imaging • Following initial stabilization • Focal injuries are readily diagnosed by CT • Patients with DAI may have normal CT scans • Most common finding is diffuse cerebral swelling

    35. Subdural hematoma www.neurosurgery.com.sg

    36. Epidural hematoma http://www.hawaii.edu/medicine/pediatrics/pemxray/v5c07.html.

    37. http://uwmedicine.washington.edu/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subid=83http://uwmedicine.washington.edu/patient-care/our-services/medical-services/stroke-center/pages/articleview.aspx?subid=83

    38. Diffuse Axonal Injury (on MRI) http://neuroradiologyonthenet.blogspot.com/2008/05/diffuse-axonal-injury-dai.html

    39. Management

    40. Goals • Minimize ICP elevation • Maintain adequate CPP to prevent secondary ischemic injury • CPP goal for adults should be 60 – 70 mmHg • Minimum acceptable for children is not defined, but recommended 40 – 65 mmHg depending on age. • Studies show that CPP from 40 – 65 improves outcome • CPP < 40 associated with poor outcome • ICP goal typically < 20 mmHg Adelson PD. PCCM. 2003

    41. Initial Decisions • Immediate NSGY consultation • Quickly identify focal injuries that require neurosurgical intervention • GCS ≤ 8 or GCS 9-12 and deteriorating/not protecting airway require intubation • Recognize signs of herniation & treat if present • Assure adequate oxygenation, breathing, BP • Give hyperosmolar therapy • Provide mild hyperventilation • Immediate NSGY evaluation

    42. Airway & Breathing • Advanced airway management necessary if • Decreasing level of consciousness (GCS ≤ 8) • Marked respiratory distress • Hemodynamic instability • Other considerations • C-spine immobilization must be maintained • Nasotracheal intubation contraindicated with midface trauma or basilar skull fracture • Cuffed tubes to protect from aspiration

    43. Rapid Sequence Intubation • Pretreat with lidocaine to minimize increase in ICP • Preoxygenation • Etomidate & Thiopental have neuroprotective properties • ? Risk of increased ICP with succinylcholine • Rocuronium may be preferred Avoid high PEEP and PIP because they will increase intrathoracic pressure and may impede cerebral venous drainage.

    44. Monitoring • Standard VS: HR, BP, Pulse Ox • Capnography • To monitor ventilation & avoid excessive hyperventilation • ICP monitoring recommended for abnormal head CT & initial GCS 3 – 8 • Interventions used to decrease ICP require accurate and continuous ICP monitoring!!

    45. ICP Monitoring • Indications • Traumatic brain injury (GCS < 8 with focal findings on CT) • Obstructive intracranial lesion • Post operative edema • Contraindications • Coagulopathy: i.e. high risk of hemorrhage • Relative Indications • Metabolic cerebral edema

    46. External Ventricular Device (EVD) both diagnostic and therapeutic Intra-parenchymal device: Diagnostic guide to therapy Others: diagnostic ICP Monitoring Options

    47. Management of ICP • First tier therapies • Maintain CPP • Sedation & analgesia • HOB at 30 degrees • Ventriculostomy drain • Neuromuscular blockade • Hyperosmolar therapy (mannitol & hypertonic saline) • Mild hyperventilation • Second tier therapies • Hyperventilation • Decompressive craniectomy • High dose barbiturates • Hypothermia (32 – 34 degrees)