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Traumatic Brain Injury 1.6 million head injuries in US annually 250,000 hospital admissions 60,000 deaths 70,000 - 90,000 permanent neurologic disabilities.

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Presentation on theme: "Traumatic Brain Injury 1.6 million head injuries in US annually 250,000 hospital admissions 60,000 deaths 70,000 - 90,000 permanent neurologic disabilities."— Presentation transcript:

1 Traumatic Brain Injury 1.6 million head injuries in US annually 250,000 hospital admissions 60,000 deaths 70,000 - 90,000 permanent neurologic disabilities Causes – Motor vehicle accidents – Falls

2 Primary Survey 1.Stabilize the spine 2.Establish adequate airway 3.Ensure adequate ventilation 4.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 12 moderate – 8 or less severe Assess strength, sensation


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;34:216-222 **Jones PA, J Neurosurg Anesth 1994;6:4-14


9 Basic Premises: 1. Monro-Kellie hypothesis  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


11 Basic Premises: 1.Monro-Kellie hypothesis 2. Compliance 3. Cerebral autoregulation

12 Intact autoregulation Lang et al JNNP 2003;74:1053-1059

13 Intact autoregulation

14 Lang et al JNNP 2003;74:1053-1059

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. 50-70 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 70-100 mm Hg  Adequate 50-60 mm Hg  Ischemia 30-40 mm Hg

19 High MAP WARNING ! ↑ in BP may be a sign of ↑ICP DO NOT TREAT/OVERTREAT BP alone CPP = MAP - ICP 70 = 75 - 5 70 mm Hg = ↑ ← ↑ 70 = 110 - 40 35 = 75 - 40

20 Cerebral perfusion pressure  CPP=MAP-ICP  Current AANS guidelines specify ICP <20 & CPP of 50-70 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% O 2 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 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 Ventriculostomy – GOLD STANDARD Drain CSF Excellent fidelity of waveform – Contraindicated: significant shift Coagulopathy – Place drain through frontal horn into lateral ventricle via burr hole Subarachnoid Bolt – No CSF drainage – less accurate as ICP rises



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 SjVO 2 > 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


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

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

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 25-30 mm Hg can cause significant vasoconstriction and reduction in cerebral blood flow Coles JP, Crit Care Med 2002;30:1950-1959 Diringer MN. J Neurosurg 2002;96:103-108 Imberti R. J Neurosurg 2002;96:97-102 Muizelaar J Neurosurg 1991;75:731-739 Cold. Acta Neurochir 1989;96:100-106 Raichle, et al. Stroke 1972;3:566-575

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 – No studies demonstrate benefit – Decrease of 1 PCO 2 decreases cerebral blood flow approx 3% – Hypocapnea decreases O 2 delivery to brain and may worsen already hypoxic neurons increases O 2 extraction which may be new way to measure – JV O 2 sat >50% improves survival Oxygenation – goal PaO 2 >70

41 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 Hemodynamic


43 Marik, P. E. et al. Chest 2002;122:699-711 Cerebral autoregulation in normal subjects and patients with chronic hypertension


45 Osmotic Agents: Mannitol  Acts within 20-30 minutes  Dosage: 0.25-1 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;92:846-851.



52 McIntyre L et al JAMA 2003



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 O 2 demand – No cellular toxicity – Burst suppression by continuous EEG Hypothermia – Reduce O 2 demand – Do not actively rewarm cold patients Decompressive Craniectomy – Last resort

57 Sedation Fentanyl is analgesic of choice – 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:



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


64 Acute subdural hematoma Chronic subdural hematoma

65 Subarachnoid hemorrhage EPIDURAL HEMATOMA

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 Gilman, S. N Engl J Med 1998;338:889-896 CT in Patients with Craniocerebral Trauma Multiple Intraparenchymal hemorrhages Subarachnoid hemorrhage

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 Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518 The NEXUS Low-Risk Criteria

77 Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518 The Canadian C-Spine Rule

78 Imaging Cervical spine films – 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 Soft tissue swelling subluxation of C4-C5 with spinal cord compression

87 Compression fracture Lumbar Burst 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 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 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

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: 699 - 711. 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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