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 Krug EG et al. Am J Public Health. 2000.

 40% of those are from TBI Langlois JA et al. Centers for Disease Control & Prevention. 2006.

 Mortality between 17 – 33% White JR et al. CCM. 2001.

 Most common cause of death & disability in childhood in developed countries Krug EG et al.  3000 children die each year from TBI in the US 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

Verbal Response

Oriented (age appropriate vocalization, smiling, cooing, tracks objects) Confused, disoriented (cries, irritable) Inappropriate words (cries to pain) Incomprehensible sounds (moans to pain) No response 5 4 3 2 1

Motor Response

Follows commands Localizes pain Withdraws to pain Abnormal flexion to pain (decorticate posturing) Abnormal extension to pain (decerebrate posturing) No response

Eye Opening

Spontaneous To command To pain No eye opening 6 5 4 3 2 1 4 3 2 1

Pathophysiology

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 Lang DA. J Neurosurg 1994  Infant skull is more compliant, tolerates significant deformation without fracture Coats B. J Neurotrauma 2006  Brain atrophy begins in young adulthood and allows for more room in the adult skull for brain to expand 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

Evaluation

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

Battle Sign

Raccoon Eyes

CSF Rhinorrhea

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/modul es/pub/neurosurgery/cranials.ht

ml

Types of Herniation a) Subfalcine : uneven, one-sided expansion of a cerebral hemisphere that pushes a portion of the brain tissue (cingulate gyrus) under the falx cerebri b) Uncal: medial temporal lobe is pushed against the tentorium. Can compress brainstem in severe cases c) Central transtentoral : downward pressure centrally, can cause bilateral uncal herniation.

d) Extracranial : brain tissue pushes through an opening in the cranial cavity either surgically or by trauma e) 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

www.neurosurgery.com.sg

Subdural hematoma

http://www.hawaii.edu/medicine/pedi atrics/pemxray/v5c07.html.

Epidural hematoma

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

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

Management

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

ICP Monitoring Options

 External Ventricular Device (EVD) both diagnostic and therapeutic  Intra-parenchymal device: Diagnostic guide to therapy  Others: diagnostic

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)

Hyperventilation

   Reduces ICP May be harmful with routine use Results in hypocapnia   Vasoconstriction Decreased cerebral blood flow  Skippen P. CCM 1997.

Associated with poor outcomes among children with TBI [30] Adelson PD. Pediatr Neurosurg 1997.

 PCO2 < 30 mmHg associated with increased mortality Curry R. PCCM 2008.

 Maintain PaCO 2 between 35 – 38 mmHg unless signs of impending herniation

Initial Fluid Management

 Restore volume—Isotonic fluids preferred  Blood products as indicated   Outcomes are poor for children who are hypotensive at initial evaluation White JR. CCM 2001 Vavilala MS. J Trauma 2003 Luerssen TG. J Neurosurg 1988 Pigula FA. J Pediatr Surg 1993 Systolic blood pressure should be maintained above the 5 th percentile for age and sex at the minimum Adelson PD. PCCM. 2003  Improved outcomes for patients with initially higher blood pressure

Head Positioning

Maintain head in neutral position to avoid jugular venous obstruction As head-up position is increased, ICP may be reduced, but beyond 30 o heads-up CPP is likely compromised. Second source: Durward, QJ, Amadner, AL, Del Maestro, RF, et al: Cerebral and vascular responses to changes in head elevation in patients with intracranial hypertension, J Neurosurg 59: 938, 1983.

Sedation and Neuromuscular Blockade

 Maintain adequate analgesia to blunt response to noxious stimuli  Maintain sedation to permit controlled ventilation  Cerebral oxygen consumption may be decreased in patients receiving neuromuscular blockade Vernon DD. CCM 2000

Antiseizure Prophylaxis

  Reduces the incidence of early posttraumatic seizures among children with severe TBI Schierhout G. Cochrane Database Syst Rev 2001 Seizures increase metabolic demand and increase ICP  Leads to secondary brain injury  Retrospective studies demonstrate improved outcomes among children with TBI treated with anticonvulsants Tilford JM. CCM 2001  Recommend anticonvulsants during the first week following TBI if high risk  Penetrating skull fractures, hematomas, masses, bleeds Adelson PD et al. PCCM 2003

Temperature control

 Aggressively prevent & treat hyperthermia  Raises metabolic demand & ICP  Hypothermia decreases cerebral metabolism and may reduce CBF & ICP (Considered second tier therapy)  Controversial  One multicenter trial showed harm  Control shivering with muscle relaxants

Hyperosmolar Therapy

 Establishes an osmotic gradient between plasma and parenchymal tissue  Reduces brain water content  Extensive research shows that it effectively decreases ICP in children with TBI

Mannitol

 Decreases ICP effectively based on extensive clinical experience  Dose 0.25 – 1 g/kg IV  Adverse effects: hyperosmolarity, hypovolemia, electrolyte imbalance  Nephrotoxicity can occur, especially if patients are hypovolemic  Don’t typically use if serum osmolarity >320 Adelson PD et al. PCCM 2003.

Hypertonic Saline

     Can be administered as a bolus or as an infusion Optimal dosing not clear   3% saline commonly used as bolus of 2-6 ml/kg Continuous infusion of 0.1 – 1 ml/kg/hr also described Effective at reducing ICP in small randomized trials & observational reports Huang SJ. Surg Neurol 2006.

Does not cause profound osmotic diuresis, so decreased risk of hypovolemia Adverse effects:  Rebound intracranial hypertension  Central pontine myelinolysis (theoretical, not reported) Qureshi AI. CCM 2000.

Glucose Control

 Hyperglycemia associated with poor outcomes  Marker for severity of injury  Worsens brain tissue lactic acidosis  Recommend to keep glucose level at least less than 200 Adelson PD. PCCM 2003.

Corticosteroids

 No benefit in trauma  Large, prospective multicenter trial demonstrated increased mortality among patients with acute TBI who received steroids  Useful only for vasogenic edema from tumors because they stabilize the BBB

Barbiturate coma—second tier therapy

 Used if ICP refractory to other modalities  Pentobarbital typically used  Decreases cerebral metabolic rate and thus cerebral blood flow  May have protective effects during periods of hypoxia and/or hypoperfusion  Cardiac suppression, hypotension  Treat with fluids & inotropic support  No evidence for prophylactic use

Other second tier therapies

    Aggressive hyperventilation (PaCO2 < 30)  Recommend brain tissue oxygenation monitoring or jugular venous O2 saturation or CBF monitoring Decompressive craniectomy   Ideal patient has had no episodes of ICP > 40 before surgery, have had a GCS > 3 at some point Evolving herniation syndrome within 48 hrs of injury Lumbar CSF drainage   Not common Must have a functioning EVD in place, open basal cisterns, no mass effect or shift on CT (to avoid herniation) Hypothermia  Core temp 32 – 34 degrees  More studies needed

Management Algorithm

Adelson PD et al. PCCM 2003

Adelson PD et al. PCCM 2003

Adelson PD et al. PCCM 2003

Second Tier Therapies Adelson PD et al. PCCM 2003

Summary

 Have Neurosurgery involved EARLY  For surgical intervention & monitor placement  Keep ICP <20 mmHg  Keep CPP appropriate for age (> 40 – 60 mmHg)

References

   Vavilala MS, Waitayawinyu P, Dooney NM. Initial approach to severe traumatic brain injury in children. www.uptodate.com 2011.

Huh JW, Raghupathi R. New concepts in treatment of pediatric traumatic brain injury. Anesthesiology Clin 2009:27;213-240.

Brasher WK. Elevated intracranial pressure in children. www.uptodate.com 2011.