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Traumatic Brain Injury

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Presentation on theme: "Traumatic Brain Injury"— Presentation transcript:

1 Traumatic Brain Injury
1.6 million head injuries in US annually 250,000 hospital admissions 60,000 deaths 70, ,000 permanent neurologic disabilities Causes Motor vehicle accidents Falls

2 Primary Survey Stabilize the spine Establish adequate airway
Ensure adequate ventilation IV access to initiate volume resuscitation Avoid secondary insults to brain Hypoxia Hypotension Determine level of consciousness examine pupils

3 Secondary Survey Once relatively stable
Includes a complete neurologic examination Severity of the head injury is classified clinically by GCS 13 to 15 mild 9 to moderate 8 or less severe Assess strength, sensation

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5 Overall goal with neurologic injury
Presume injury until proven otherwise Identify early Allow injured tissue the best chance to repair itself Adequate delivery of oxygen and glucose Avoid infection Preserve residual nervous tissue

6 Primary Brain Injury Trauma: concussion, contusion,
diffuse axonal injury Ischemia: global, regional Inflammation Direct Injury: hemorrhage, penetrating injury Compression: tumor, edema, Hematoma Metabolic insults Excitatory toxicity: seizures, illicit drugs, severe hyperthermia

7 Secondary Brain Injury
Hypoperfusion: hypotension, high intracranial pressure, vasospasm Single episode SBP <90 mm Hg increases morbidity & doubles mortality* Hypoxemia* ** pO2 ≤ 60 mm Hg increases poor outcome from 28% to 71% * Increases mortality 50% from 14.3% ** Harmful mediators: reperfusion, inflammation Electrolyte changes *Chestnut RM, et al. J Trauma 1993;34: **Jones PA, J Neurosurg Anesth 1994;6:4-14

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9 Basic Premises: 1. Monro-Kellie hypothesis 2. Compliance
3 compartments: brain, blood, & CSF Increase in one must be compensated by decrease in others or the ICP will increase 2. Compliance volume to pressure relationship

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11 Basic Premises: Monro-Kellie hypothesis 2. Compliance
3. Cerebral autoregulation

12 Intact autoregulation
Lang et al JNNP 2003;74:

13 Intact autoregulation

14 Intact autoregulation
Lang et al JNNP 2003;74:

15 Defective autoregulation

16 Basic Premises: Monro-Kellie hypothesis 2. Compliance
3. Cerebral autoregulation 4. CPP = MAP – ICP

17 Optimal cerebral perfusion pressure (CPP) in patients with acute traumatic brain injury by current guidelines is: A. Maintaining a mean arterial pressure of greater than 90 mm Hg. B mm Hg. C. greater than 70 mm Hg. D. determined without an ICP monitor. E. not important, ICP is the parameter to follow

18 Cerebral perfusion pressure
CPP = MAP - ICP Normal is mm Hg Adequate mm Hg Ischemia mm Hg

19 DO NOT TREAT/OVERTREAT BP alone
High MAP WARNING ! ↑ in BP may be a sign of ↑ICP DO NOT TREAT/OVERTREAT BP alone CPP = MAP - ICP 70 = 70 mm Hg = ↑ ← ↑ 70 = 35 =

20 Cerebral perfusion pressure
CPP=MAP-ICP Current AANS guidelines specify ICP <20 & CPP of mmHg Lower CPP : poorer outcome (ischemic) Higher CPP: more ARDS J Neurotrauma. 2007; 24:S59-64

21 Initial Management – Pre-hospital
A B C D Intubate early if GCS <8 Systolic BP of < 110 requires fluid resuscitation Rapid transport to trauma center Avoid sedation if possible to preserve neuro exam

22 Early Hospital Management
Intubate if GCS <8 Rapid sequence preferred Avoid increased ICP with placement of ETT Preferred drugs Etomidate – rapid acting, short duration, min BP effect Rocuronium- short duration, no BP effect, no increased ICP 100% O2 until transferred to ICU Initial target PCO2 should be 35 to 40 mm Hg MAP goal 90 Use only LR or NS – NO HYPOTONIC FLUID

23 Maintain Oxygenation! Hypoxemia ≤ 60 mm Hg increases poor
outcome from 28% to 71% (trauma)

24 Neurosurgical consultation
CT head – non contrast All patients at risk GCS <15 Depressed skull or evidence of basilar skull fracture Focal neuro deficits GCS 15, +LOC Neurosurgical consultation Surgical evacuation all acute traumatic extra-axial hematoma >1 cm subdural or epidural hematoma > 5 mm with an equivalent midline shift and GCS<8 depressed, open, and compound skull fractures recommended if hematoma > 20 ml with mass effect

25 ICU Management Serial neurologic exams
ICP monitor recommended in patients with a GCS score < 8 intracranial HTN > 60% No RCT’s to support improved outcomes with ICP monitor Studies demonstrate outcome is inversely proportional to max ICP reading and time spent >20

26 ICP Monitoring Different sites 1) Intraventricular- Gold standard
2) Intraparenchymal 3) Subarachnoid 4) Subdural 5) Epidural Different modalities 1) Fiberoptic 2) Fluid-coupled

27 ICP Measurement Subarachnoid Bolt Ventriculostomy GOLD STANDARD
No CSF drainage less accurate as ICP rises Ventriculostomy GOLD STANDARD Drain CSF Excellent fidelity of waveform Contraindicated: significant shift Coagulopathy Place drain through frontal horn into lateral ventricle via burr hole

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30 ICP Monitors continued
Most common catheter is transducer tipped, fiber optic inserted in parenchyma via twist-drill burr hole Extradural Subdural Intraparenchymal 10% infection rate with monitors Prophylactic antibiotics not proven effective Routine site changes is not proven effective Monitors are not perfect Significant posterior fossa events can occur without changes in CSF output Catheter malfunction is common ALWAYS correlate exam

31 Intracranial Pressure
Normal <10 Elevated >20 = Intracranial HTN Cerebral Perfusion Pressure CPP = MAP – ICP CPP <70 associated with less favorable outcome Intracranial compliance - minimal Intracranial vault contents

32 Jugular Venous Oximetry
Continuous SjVO2 Blood Draws for CvO2 Value Normal Ischemia SjVO2 > 60% <50% (10 min.)

33 Tissue PO2 Monitoring: Pbto2 Licox- Integra
Direct measurement of tissue oxygen tension (?) Local measurement Part of ICP-bolt system Experimental use in Europe since 1992 Approved for use in Europe, Canada, and US

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35 Management of Intracranial HTN
3 targets Intracranial blood volume reduction CSF drainage Brain parenchyma reduction

36 Cerebral blood volume Increase Decrease Ischemia
Acidosis Hypercapnia Increased venous pressure Hyperthermia Decrease Elevate head to 30 degrees Midline position of head Sedation Muscle relaxation Decrease airway pressure

37 Hyperventilation Begins almost immediately Peak effect in 30 minutes
Lowers ICP by 25-30% in most patients May decrease cerebral blood flow: No lower than pCO2 of 30mm Hg Normalize within hours

38 Ventilation: Hyperventilation
PaCO2 of mm Hg can cause significant vasoconstriction and reduction in cerebral blood flow Coles JP, Crit Care Med 2002;30: Diringer MN. J Neurosurg 2002;96: Imberti R. J Neurosurg 2002;96:97-102 Muizelaar J Neurosurg 1991;75: Cold. Acta Neurochir 1989;96: Raichle, et al. Stroke 1972;3:

39 Hyperventilation Hyperventilation lowers CBF, and therefore ICP, by raising the extracellular pH in the CNS CO2 is not the direct mediator of this response Hyperventilation does not ‘stop working;’ however, The choroid plexus exports bicarbonate to lower the pH 6 hour time course The cause of the ICP elevation is usually progressive Further attempts at hyperventilation will raise intrathoracic pressure, decreasing jugular venous return and thereby raising ICP

40 CBV continued Hyperventilation Oxygenation – goal PaO2 >70
No studies demonstrate benefit Decrease of 1 PCO2 decreases cerebral blood flow approx 3% Hypocapnea decreases O2 delivery to brain and may worsen already hypoxic neurons increases O2 extraction which may be new way to measure – JV O2 sat >50% improves survival Oxygenation – goal PaO2 >70

41 Hemodynamic CBF is independent of MAP between 50-150 Autoregulation
With injury 50% pts lose autoregulation ability GOAL – Normal MAP or MAP >90 Treat hypotension with thoughts of cause Treat HTN with B-blockers, nicardipine Use vasodilators with caution

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43 Cerebral autoregulation in normal subjects and patients with chronic hypertension
Marik, P. E. et al. Chest 2002;122:

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45 Osmotic Agents: Mannitol
Acts within minutes Dosage: g/kg bolus Filtered needles! Actions: 1) osmotic gradient 2) may increase cardiac preload, output and elevate MAP 3) improves rheology of red blood cells 4) decreases CSF production 5) free radical scavenger

46 Osmotic Agents: Mannitol
Serum osmolality <320 mOsm/L vs osmolar gap <10 Measured osmoles – (2Na +glu/18+BUN/2.8) Watch for osmotic diuresis: Dehydration and hypotension MAINTAIN EUVOLEMIA

47 Brain parenchyma reduction if CSF drainage not possible or ineffective
Mannitol Osmotic duiretic, draws out fluid from brain Likely from normal brain tissue Increases CBF but decreases ICP Follow serum Osm and Na No mannitol if >315 Follow for dehydration, hypotension, and prerenal azotemia Bolus administration Steroids – no benefit

48 Hypertonic Saline 3% saline 250cc bolus (run in as fast as possible)
7% saline bolus 23.4% saline 30cc bolus

49 Fever Each increase in 1degree Celsius increases cerebral metabolic rate by 7% One study w/ exercise: 1.5º C increased CMRO2 by 23% increase in CMRO2 Vasodilation CBV ICP Increases O2 requirements Increases CO2 production (may need to adjust ventilator minute ventilation!!!) Nunnely SA et al. J Appl Physiol 2002;92:

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52 McIntyre L et al JAMA 2003

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55 Pentobarbital coma may result in:
A. hyperthermia. B. hypertension. C. increased respiratory drive. D. unreactive large pupils. E. increased electrographic activity

56 Additional methods to decrease ICP for when conventional management fails No demonstrated benefit
Barbiturate coma Reduce O2 demand No cellular toxicity Burst suppression by continuous EEG Hypothermia Do not actively rewarm cold patients Decompressive Craniectomy Last resort

57 Sedation Fentanyl is analgesic of choice Propofol
Min BP effect, depresses cough Propofol easily titratable, rapidly reversible decreases cerebral metabolic rate Potentiates GABA inhibition Inhibitions methyl-D-aspartate glutamate receptors Inhibits voltage-dependent calcium channels Potent antioxidant Inhibits lipid peroxidation Can paralyze if needed, but keep to minimum

58 Seizure Prophylaxis Anti-seizure medication
7 days after severe injury Usually phenytoin Avoid abnormal electrolytes Hyponatremia SIADH Cerebral salt wasting Hypomagnesemia

59 Hemicraniectomy:

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62 4 types of acute post-traumatic intracranial hemorrhage:
Subarachnoid hemorrhage Periventricular and frontal lobe contusions with intraparenchymal hematoma Subdural hematoma EPIDURAL HEMATOMA Mattiello, J. A. et al. N Engl J Med 2001;344:580

63 EPIDURAL HEMATOMA

64 Acute subdural hematoma Chronic subdural hematoma

65 EPIDURAL HEMATOMA Subarachnoid hemorrhage

66 Multiple intraparenchymal hematomas with surrounding edema

67 Diffuse Axonal Injury May cause immediate and prolonged unconsciousness High morality, high morbidity, often persistent vegetative state Identified by diffusion-weighted MRI Caused by shearing forces affecting axons leading to dysfunction of the reticular activating system Axons are not torn but sequential, focal changes that lead to swelling and disconnection over multiple hours Apoptosis may play role in axonal injury

68 CT in Patients with Craniocerebral Trauma
Multiple Intraparenchymal hemorrhages Figure 4. CT in Patients with Craniocerebral Trauma. Panel A is a CT scan demonstrating multiple intraparenchymal hemorrhages consistent with the occurrence of extensive shearing injuries in a 70-year-old woman who was the unrestrained driver of a car that struck a tree. Subarachnoid hemorrhage is also present (arrow). Panel B is a CT scan revealing acute epidural hematoma (arrowheads), intracranial air (black arrow), and a skull fracture (curved arrow) in a 44-year-old man with deteriorating mental status who struck his head falling out of bleachers 12 hours before imaging. Panel C is a CT scan showing a right-sided crescentic acute subdural hematoma (arrows) with mass effect on midline structures in a 50-year-old man with a history of drug abuse and alcoholic cirrhosis who presented with the sudden onset of unresponsiveness. Subarachnoid hemorrhage Gilman, S. N Engl J Med 1998;338:

69 Depressed skull fracture

70 Poor prognosis Advanced age Female <50
Anticoagulation at time of trauma Low GCS at arrival Hypotension Abnormal pupillary widening Traumatic SAH

71 Things to keep in mind… Spine injury until proven otherwise
Many intraparenchymal hematomas may be delayed, appearing on the CT scan 24 h after the initial insult Low threshold to repeat CT scan Clinical changes Continued uncontrollable intracranial HTN

72 Acute Spinal Injury 10,000 new cases annually Males 16-30 make up 80%
Most due to MVA 36%, violence 29%, falls 21% Quadriplegia is slightly more common than paraplegia Rare to completely transect cord 6-8% of head trauma will also have spine injury Main goal is early identification Insult is associated with an injury response that results in neuronal destruction

73 Secondary injury cascade of tissue injury
vascular compromise inflammatory changes cellular dysfunction free radical generation hallmark is spinal cord edema peaks 3 to 6 days after injury subsides over a period of weeks

74 Initial Resuscitation
Regular ABC’s Immobilize neck until cleared or stabilized Head between two sandbags Placement of cervical collar Immobilize entire spine Transportation on a rigid spine board Log rolling 25-50% of cervical spine injuries also have head injury

75 Neurologic exam Early Sequential Include
Strength Sensation – pain, position Neurologic level: most caudal segment of the spinal cord with normal bilateral motor (strength >3/5) and sensory (light touch and pinprick) function

76 The NEXUS Low-Risk Criteria
Table 1. The NEXUS Low-Risk Criteria. Stiell, I. G. et al. N Engl J Med 2003;349:

77 The Canadian C-Spine Rule
Figure 1. The Canadian C-Spine Rule. For patients with trauma who are alert (as indicated by a score of 15 on the Glasgow Coma Scale) and in stable condition and in whom cervical-spine injury is a concern, the determination of risk factors guides the use of cervical-spine radiography. A dangerous mechanism is considered to be a fall from an elevation [>=]3 ft or 5 stairs; an axial load to the head (e.g., diving); a motor vehicle collision at high speed (>100 km/hr) or with rollover or ejection; a collision involving a motorized recreational vehicle; or a bicycle collision. A simple rear-end motor vehicle collision excludes being pushed into oncoming traffic, being hit by a bus or a large truck, a rollover, and being hit by a high-speed vehicle. Stiell, I. G. et al. N Engl J Med 2003;349:

78 Imaging Cervical spine films CT scan – best for bones MRI
AP, lateral, and odontoid Additional laterals If entire c-spine or C7–T1 space not seen Abnormal vertebral alignment, bony structure, intervertebral space, and soft tissue thickening Flexion and extension films SCIWORA (spinal cord injury without radiologic abnormality) CT scan – best for bones If not adequate visualization by X-ray MRI Modality of choice for characterizing acute cord injury Best for edema, hemorrhage, ligamentous injury

79 Neuroresuscitative Agents
High dose steroids 30mg/kg bolus 5.4mg/kg/hr x 23H Give for 48H if not given within 3H Effective if given in first 8 hours

80 Injury classification
Stable Unstable Soft tissue or fracture Surgery Decompress neural tissue Prevent cord injury by ensuring stability Options include bed rest in traction (rarely done) external immobilization open reduction with internal fixation

81 Order of injury Repair Any open fractures first
Then any closed fracture Tibia Femur – within 24h Pelvis Spine Upper extremity

82 Ligamentous injury

83 Odontoid Fracture Atlas fracture

84 C2 Hangman’s Fracture

85 C6 Fracture with retropulsion
to cord

86 subluxation of C4-C5 with spinal cord compression
Soft tissue swelling

87 Lumbar Burst fracture Compression fracture

88 Cord Injury Syndromes Complete cord lesion - all sensory and motor function below the lesion is abolished Central cord lesion – motor function lost upper>lower suspended sensory loss in cervicothoracic dermatomes Posterior Cord syndrome – diminished proprioception and fine touch Brown-Sequard syndrome - cord hemisection ipsilateral loss of pain and proprioception, contralateral pain and temp loss, suspended ipsilateral loss of all sensation Spinal shock – lack of neurologic function after trauma that can last until 4 weeks

89 Systemic Effects of SCI
Respiratory Related to level of injury Thoracic levels eliminates intercostals Diaphragm alone to inspire – phrenic nerve (C3-5) Cervical lesions decreases cough and secretion clearance Decreased tidal volumes Minimal expiratory help Status improves with time Cardiovascular Almost solely related to interruption of sympathetic pathway at T1-L2 Bradycardia Resolves with stimulation Resolves after 2 months Rare to need pacemaker Hypotension Give volume Low dose pressors

90 Autonomic hyperreflexia
Loss of central inhibition hyper-reactive sympathetic reflexes to cord below level of lesion Bladder or bowel distention usual causes HTN Arrythmias Headaches Vasodilation above lesion level

91 In Summary Appropriate pre-hospital care is essential Assume injury until proven otherwise Evaluate as early as possible to prevent unnecessary immobilization Earlier steroids with spinal injury Follow clinical exam

92 References Czosnyka M. Pickard JD. Monitoring and interpretation of intracranial pressure. Journal of Neurology, Neurosurgery & Psychiatry. 75(6):813-21, 2004 Jun. Gunnarsson T. Fehlings MG. Acute neurosurgical management of traumatic brain injury and spinal cord injury. Current Opinion in Neurology. 16(6):717-23, 2003 Dec. Hutchinson PJ. Kirkpatrick PJ. Decompressive craniectomy in head injury. Current Opinion in Critical Care. 10(2):101-4, 2004 Apr Longhi L. Stocchetti N. Hyperoxia in head injury: therapeutic tool?. Current Opinion in Critical Care. 10(2):105-9, 2004 Apr Marik, PE. Varon, J. and Trask, T Managament of Head Trauma*Chest. 2002; 122: Marshall LF. Head injury: recent past, present, and future. Neurosurgery. 47(3):546-61, 2000 Sep Patel RV. DeLong W Jr. Vresilovic EJ. Evaluation and treatment of spinal injuries in the patient with polytrauma.Clinical Orthopaedics & Related Research. (422):43-54, 2004 May.


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