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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 Causes Motor vehicle accidents Falls. Primary Survey. Stabilize the spine Establish adequate airway E nsure adequate ventilation

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Traumatic brain injury
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


Primary survey
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


Secondary survey
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


Overall goal with neurologic injury
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


Primary brain injury
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


Secondary brain injury
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 NeurosurgAnesth 1994;6:4-14


Basic premises
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


Basic premises1
Basic Premises:

  • Monro-Kellie hypothesis

  • 2. Compliance

  • 3. Cerebral autoregulation


Intact autoregulation
Intact autoregulation

Lang et al JNNP 2003;74:1053-1059



Intact autoregulation2
Intact autoregulation

Lang et al JNNP 2003;74:1053-1059



Basic premises2
Basic Premises:

Monro-Kellie hypothesis

2. Compliance

3. Cerebral autoregulation

4. CPP = MAP – ICP


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


Cerebral perfusion pressure
Cerebral perfusion pressure acute traumatic brain injury by current guidelines is:

  • CPP = MAP - ICP

  • Normal is 70-100 mm Hg

  • Adequate 50-60 mm Hg

  • Ischemia 30-40 mm Hg


High map
High MAP acute traumatic brain injury by current guidelines is:

  • 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


Cerebral perfusion pressure1
Cerebral perfusion pressure acute traumatic brain injury by current guidelines is:

  • 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


Initial management pre hospital
Initial Management – Pre-hospital acute traumatic brain injury by current guidelines is:

  • 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


Early hospital management
Early Hospital Management acute traumatic brain injury by current guidelines is:

  • 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


Maintain oxygenation
Maintain Oxygenation! acute traumatic brain injury by current guidelines is:

  • Hypoxemia ≤ 60 mm

    Hg increases poor

    outcome from 28%

    to 71% (trauma)


  • CT head – non contrast acute traumatic brain injury by current guidelines is:

    • 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


Icu management
ICU Management acute traumatic brain injury by current guidelines is:

  • 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


Icp monitoring
ICP Monitoring acute traumatic brain injury by current guidelines is:

  • Different sites

    1) Intraventricular-

    Gold standard

    2) Intraparenchymal

    3) Subarachnoid

    4) Subdural

    5) Epidural

  • Different modalities

    1) Fiberoptic

    2) Fluid-coupled


Jugular venous oximetry
Jugular Venous Oximetry acute traumatic brain injury by current guidelines is:

  • Continuous SjVO2

  • Blood Draws for CvO2

Value Normal Ischemia

SjVO2 > 60% <50% (10 min.)


Tissue po2 monitoring pbto2 licox integra
Tissue PO2 Monitoring: acute traumatic brain injury by current guidelines is: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


Management of intracranial htn
Management of Intracranial HTN acute traumatic brain injury by current guidelines is:

  • 3 targets

    • Intracranial blood volume reduction

    • CSF drainage

    • Brain parenchyma reduction


Cerebral blood volume

Decrease acute traumatic brain injury by current guidelines is:

Elevate head to 30 degrees

Midline position of head

Sedation

Muscle relaxation

Decrease airway pressure

Increase

Ischemia

Acidosis

Hypercapnia

Increased venous pressure

Hyperthermia

Cerebral blood volume


Hyperventilation
Hyperventilation acute traumatic brain injury by current guidelines is:

  • 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


Ventilation hyperventilation
Ventilation: Hyperventilation acute traumatic brain injury by current guidelines is:

  • 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. ActaNeurochir 1989;96:100-106

    Raichle, et al. Stroke 1972;3:566-575


Hyperventilation1
Hyperventilation acute traumatic brain injury by current guidelines is:

  • 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


Hemodynamic acute traumatic brain injury by current guidelines is:

  • 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


Cerebral autoregulation in normal subjects and patients with chronic hypertension

Marik, P. E. et al. Chest 2002;122:699-711


Osmotic agents mannitol
Osmotic Agents: Mannitol chronic hypertension

  • 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


Osmotic agents mannitol1
Osmotic Agents: Mannitol chronic hypertension

  • Serum osmolality <320 mOsm/L vsosmolar gap <10

  • Measured osmoles –

    (2Na +glu/18+BUN/2.8)

  • Watch for osmotic diuresis: Dehydration and hypotension

  • MAINTAIN EUVOLEMIA


Hypertonic saline
Hypertonic Saline chronic hypertension

  • 3% saline 250cc bolus (run in as fast as possible)

  • 7% saline bolus

  • 23.4% saline 30cc bolus


Fever
Fever chronic hypertension

  • 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!!!)

    NunnelySA et al. J ApplPhysiol 2002;92:846-851.


McIntyre L et al JAMA 2003 chronic hypertension


Pentobarbital coma may result in
Pentobarbital coma may result in: chronic hypertension

A. hyperthermia.

B. hypertension.

C. increased respiratory drive.

D. unreactive large pupils.

E. increased electrographic activity


Additional methods to decrease icp for when conventional management fails no demonstrated benefit

Barbiturate coma chronic hypertension

Reduce O2 demand

No cellular toxicity

Burst suppression by continuous EEG

Hypothermia

Reduce O2 demand

Do not actively rewarm cold patients

Decompressive Craniectomy

Last resort

Additional methods to decrease ICPfor when conventional management failsNo demonstrated benefit


Sedation
Sedation chronic hypertension

  • 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


Seizure prophylaxis
Seizure Prophylaxis chronic hypertension

  • Anti-seizure medication

    • 7 days after severe injury

    • Usually phenytoin

  • Avoid abnormal electrolytes

    • Hyponatremia

      • SIADH

      • Cerebral salt wasting

    • Hypomagnesemia


Hemicraniectomy
Hemicraniectomy: chronic hypertension


4 chronic hypertension 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


EPIDURAL HEMATOMA chronic hypertension


Acute chronic hypertension

subdural

hematoma

Chronic

subdural

hematoma


EPIDURAL HEMATOMA chronic hypertension

Subarachnoid

hemorrhage


Multiple chronic hypertension

intraparenchymal

hematomas with

surrounding edema


Diffuse axonal injury
Diffuse Axonal Injury chronic hypertension

  • 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


CT in Patients with Craniocerebral Trauma chronic hypertension

Multiple

Intraparenchymal

hemorrhages

Subarachnoid

hemorrhage

Gilman, S. N Engl J Med 1998;338:889-896


Depressed skull chronic hypertension

fracture


Poor prognosis
Poor prognosis chronic hypertension

  • Advanced age

  • Female <50

  • Anticoagulation at time of trauma

  • Low GCS at arrival

  • Hypotension

  • Abnormal pupillary widening

  • Traumatic SAH


Things to keep in mind
Things to keep in mind… chronic hypertension

  • 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


Acute spinal injury
Acute Spinal Injury chronic hypertension

  • 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


Secondary injury
Secondary injury chronic hypertension

  • 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


Initial resuscitation
Initial Resuscitation chronic hypertension

  • 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


Neurologic exam
Neurologic exam chronic hypertension

  • 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


The NEXUS Low-Risk Criteria chronic hypertension

Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518


The Canadian C-Spine Rule chronic hypertension

Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518


Imaging
Imaging chronic hypertension

  • 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


Neuroresuscitative agents
Neuroresuscitative Agents chronic hypertension

  • 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


Injury classification chronic hypertension

  • 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


  • Order of injury repair
    Order of injury Repair chronic hypertension

    • Any open fractures first

    • Then any closed fracture

      • Tibia

      • Femur – within 24h

      • Pelvis

      • Spine

      • Upper extremity


    Ligamentous injury chronic hypertension


    Odontoid Fracture chronic hypertension

    Atlas fracture


    C2 Hangman’s Fracture chronic hypertension


    C6 Fracture with retropulsion chronic hypertension

    to cord


    subluxation of C4-C5 with chronic hypertension

    spinal cordcompression

    Soft tissueswelling


    Lumbar chronic hypertension

    Burst

    fracture

    Compressionfracture


    Cord injury syndromes
    Cord Injury Syndromes chronic hypertension

    • 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 hemisectionipsilateral 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


    Systemic effects of sci

    Cardiovascular chronic hypertension

    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

    Systemic Effects of SCI


    Autonomic hyperreflexia
    Autonomic hyperreflexia chronic hypertension

    • 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


    In summary
    In Summary chronic hypertension

    • 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


    References
    References chronic hypertension

    • 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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