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
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.
GCS • Severity of TBI is defined by the GCS Score • Mild • GCS 13-15 • Moderate • GCS 9-12 • Severe • GCS <9
GCS Total score ranges from 3 - 15
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
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
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
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
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.
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).
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
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
Cerebral Autoregulation • Often impaired in children with TBI • Impaired autoregulation is associated with worse outcome Cerebral autoregulation in hypertension Kaplan, NM, Lancet 1994
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
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
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
Initial Evaluation • Don’t forget standard trauma protocols: • Primary Survey • ABCs! • Secondary Survey
History • Mechanism of injury • Loss of consciousness + duration • Vomiting • Headache • One of the earliest symptoms of increased ICP • Progression of symptoms
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
Neuro exam • Assign a GCS • Level of consciousness • Pupils • Extraocular movements • Funduscopic exam • Brainstem reflexes • DTRs • Response to pain
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.
Funduscopic Exam www.dontshake.org http://cloud.med.nyu.edu/modules/pub/neurosurgery/cranials.html
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
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!!
Mydriasis • Can be associated with CN III injury • Uncal herniation can cause unilateral mydriasis & ptosis
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.
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
Subdural hematoma www.neurosurgery.com.sg
Epidural hematoma http://www.hawaii.edu/medicine/pediatrics/pemxray/v5c07.html.
Diffuse Axonal Injury (on MRI) http://neuroradiologyonthenet.blogspot.com/2008/05/diffuse-axonal-injury-dai.html
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
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
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
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.
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!!
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
External Ventricular Device (EVD) both diagnostic and therapeutic Intra-parenchymal device: Diagnostic guide to therapy Others: diagnostic ICP Monitoring Options
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)