2. Objectives
• To discuss the basic neurologic examination for TBI
patients at the emergency room
• To emphasize important and alarming physical exam
findings for TBI patients
• To discuss the diagnostic and therapeutic algorithm for
TBI patients
3. • Brain damage resulting from external forces
because of direct impact, rapid acceleration
or deceleration, penetrating object or blast
waves from an explosion
Traumatic Brain Injury
Theadom et al 2017
4. Traumatic Brain Injury
Primary Injury Secondary Injury
Acute consequences of
tissue loading leading to
tissue deformation
Pathophysiologic
sequelae
28. Initial Resuscitation
Hudgens and Grady, 2017
Advanced Trauma Life Support Guidelines 2018
Primary Survey Secondary Survey
A-irway
B-reathing
C-irculation
D-isability
E-xposure
+ Adjunct diagnostics
A-llergies
M-edications
P-ast Medical Hx
L-ast meal
E-vents/Examination
+ Adjunct diagnostics
29. Advanced Trauma Life Support Guidelines 2018
✅ ✅ plain cranial CT (within 30 minutes)
✅ ✅ trauma series x-rays (chest, pelvis, hip)
✅ ✅ FAST
✅ “man scan”: cervical, chest, abdominal CT
✅ extremity x-rays as needed
30. Stiel et al 2001
Canadian Head CT rule
(for mild TBI)
Inclusion criteria:
• minor head trauma with
loss of consciousness
• GCS 13-15
• confusion
• amnesia after event
Exclusion criteria:
• anticoagulant use
• age <16 year
• seizure
31. Stiel et al 2001
HIGH RISK FACTORS
⚠️ failure to reach GCS 15
within 2 hours
⚠️ suspected open skull
fracture
⚠️ any sign of basal skull
fracture
⚠️ ≥ vomiting epsisodes
⚠️ ≥ 65 years
MEDIUM RISK
FACTORS
⚠️ amnesia after
impact >30 minutes
⚠️ dangerous
mechanism of injury
(pedestrian vs vehicle,
ejected from vehicle, fall
from ≥3feet or 5 stairs)
Proceed with Cranial CT
32. Patient Position
Peterson et al, 2008
Aisiku et al, 2017
• Elevate head of bed to 30 degrees minimize
venous outflow resistance decrease ICP
• Keep neck in neutral position
• Immobilize cervical spine until proven to have no
fractures
33. Fluid Resuscitation
Hudgens and Grady, 2017
• Administer an initial, warmed bolus of isotonic fluid
• Adults: 1 liter, Children <40kg: 20ml/kg
• Maintain SBP ≥ 100 mm Hg for 50 to 69 years*
• Maintain SBP ≥ 110 mm Hg for 15 to 49 years or older
than 70 years*
34. Continuous Reevaluation
Advanced Trauma Life Support Guidelines 2018
• Re-examination, vital signs monitoring
• Ensure adequate analgesia
• Maintain urine output 0.5ml/kg/hr for
adults and 1ml/kg/hr for pediatric patients
35. Ventilation Therapy
Brain Trauma Foundation Guidelines, 2016
• Severe TBI patients require definitive airway
protection endotracheal intubation
• Hyperventilation is recommended as temporizing
measure for ICP reduction
• Prolonged prophylactic hyperventilation in patients
with PaCO2 of ≤25mmHg is NOT recommended
36. Hyperosmolar Therapy
MANNITOL (20%) HYPERTONIC SALINE
MOA Creation of osmotic gradient
Osmotic diuretic
Reduction of blood viscosity
Creation of osmotic gradient
Plasma expander
Reduction of blood viscosity
Dose 0.25g/kg to 1g/kg body weight Bolus dose* Continuous infusion
Timing Onset within 1-5 minutes
Peak 20-60 minutes
Duration 1.5-6hours
Peak 10 minutes
Duration 1hour
Depends on rate, and
if serum sodium
target is reached
Adverse
effects
Dehydration
Hypotension
Rebound cerebral edema
Hyperchloremic metabolic acidosis
Thrombophlebitis
Contra-
indications
Established anuria, pulmonary
congestion/edema, active internal
bleeding, severe dehydration, allergy to
Mannitol
None known according to FDA
Use with caution in patients with renal
insufficiency or heart failure
40. Sedation and Analgesia
• Benzodiazepines cause a coupled reduction in
CMRO2 and CBF, with no effect on ICP
• Narcotics have no effect on CMRO2 or CBF but have
been reported to increase ICP in some patients
• Dexmedetomidine (0.2 to 0.7 μg/hr) provides
adequate sedation without altering respiratory drive
Aisiku et al, 2017
Brain Trauma Foundation Guidelines, 2016
41. Sedation and Analgesia
• High-dose barbiturate recommended to control
elevated refractory ICP
• Propofol (1-2mg/kg initial IV, 5-50 μg/kg/min
maintenance) may be given for ICP control, but not
at high doses (>100mg/kg for >48hrs)
Aisiku et al, 2017
Brain Trauma Foundation Guidelines, 2016
43. Nutrition and Fluids
• Feed patients by 5th day (at most by 7th day) post-
injury to decrease mortality*
• Continuous vs. bolus feeding
• Transgastric jejunal feeding is recommended to
reduce VAP
• Maintenance fluids 35ml/kg/day
• Administer proton pump inhibitor
Aisiku et al, 2017
Brain Trauma Foundation Guidelines, 2016
44. Infection Prophylaxis
• Early tracheostomy reduces mech vent days and
decreases ICU stay
• Prophylactic antibiotics for pneumonia not
recommended at this time
• Nursing care for contraptions
Brain Trauma Foundation Guidelines, 2016
45. Post-traumatic seizures
• Early PTS: within 7 days of injury
• Late PTS: after 7 days of injury
• Phenytoin recommended to decrease incidence of
early PTS
• Emerging role of Levetiracetam
• Seizure prophylaxis still controversial*
Brain Trauma Foundation Guidelines, 2016
46. Deep Vein Thrombosis
• Risk for VTE due to prolonged immobilization,
motor deficits, hypercoagulability
• Mechanical prophylaxis is equally effective
• May give LMWH as soon as safe (stable bleed on
serial scans)
Brain Trauma Foundation Guidelines, 2016
47. Fever
• Fever is a significant source of secondary injury
associated with worse outcome
• Each degree Celsius elevation cerebral
metabolism increases by 10-13%
Shalaieh et al 2017
48. Prophylactic Hypothermia
• Neuroprotective and ICP-lowering effects
• Maintaining Temp 35.0-35.5 degrees maximally
reduces ICP while maintaining CPP, cardiac dynamics
and oxygen delivery
• Early (within 2.5hrs) and short-term (48hrs post-
injury) prophylactic hypothermia is not
recommended to improve outcomes
Aisiku et al, 2017
Brain Trauma Foundation Guidelines, 2016
49. Do steroids have a role in TBI?
• No. Steroids are not recommended for improving
outcome or reducing ICP
Brain Trauma Foundation Guidelines, 2016
51. Diffuse Axonal Injury
• results from severe angular and rotational
acceleration and deceleration that delivers
shear and tensile forces to axons
• severe impairment despite lack of gross
injuries
• Strich hemorrhages
52. Diffuse Axonal Injury
• definitively diagnosed in post-mortem
pathologic exam of brain tissue
• diagnosed after TBI with GCS <8 for more
than 6 consecutive hours
Heterogeneous disorder with different forms of presentation, defined as Brain damage resulting from external forces as a consequence of direct impact, rapid acceleration or deceleration, penetrating object or blast waves from an explosion.
The nature, intensity, direction and duration of these forces determine the extent of damage.
Primary injury: damage stemming from mechanical forces occurring at the time of the traumatic insult
Focal injuries are defined as visible damage to the parenchyma that is generally limited to a well-circumscribed region; examples of focal injuries include contusions to the cortex and subdural, epidural, and intracerebral hematomas.
Diffuse brain injuries differ from focal brain injuries and skull fracture in that they often occur without producing macroscopic structural damage, are associated with widespread brain dysfunction, and appear in approximately 40% of patients with severe brain injuries.
------
Secondary injury: complex series of interrelated molecular processes initiated by the primary injury that causes progressive loss of CNS cells for weeks and months after the primary injury has ceased
We are all familiar with the Glasgow Coma Scale which was devised back in the 1970s
TBI is classified as mild when the GCS is 14-15, moderate when the GCS is 9-13 and Severe when the GCS is 3-8.
Clinical severity of intracranial injuries is commonly assessed according to the degree of depression of the level of consciousness, assessed by the Glasgow Coma Scale (GCS).14 The GCS score is the sum score (range, 3-15) of three components (eye, motor, and verbal scales), each of which is used to assess different aspects of reactivity. The motor component provides more discrimination in patients with severe injuries, whereas the eye and verbal scales are more dis- criminative in patients with moderate and mild injuries.
A limitation of classifying clinical severity with the GCS is that assessment may be confounded by prior alcohol or substance use, prehospital sedation, paralysis, and intubation
This system is based on a five-interval severity classification (minimal through critical), determined primarily by the initial post-resuscitation Glasgow Coma Scale score.
The HISS is proposed as a framework on which further research can be done to guide care to predict outcome and to perform audits on head-injured patients.
In this part of my presentation, I will now elucidate the pathophysiology of traumatic brain injury in this patient, and highlight the pearls in her medical and surgical management
The initial management of any trauma is based on the 2018 ATLS guidelines
The primary survey will ensure that all life-threatening issues are assessed systematically – simultaneous resuscitation
Airway must be assessed and secured while maintaining the spine in a neutral position
Breathing – pt must be administered with high-flow O2, chest must be assessed for injuries (recognize and tx tension pneumothorax, massive hemothorax, flail chest, sucking chest wounds, pericardial tamponade)
Circulation – look for external hemorrhage (scalp lacerations), observe skin color, temperature and capillary refill, feel the pulse, record BP, assess neck veins
Disability – GCS, pupil exam, brainstem exam, examine for lateralizing signs of SCI
Exposure – expose the pt for adequate examination, log roll, prevent hypothermia
Adjunct exams: electrocardiography, pulse oximetry, carbon dioxide (CO2) monitoring, and assessment of ventilatory rate, and arterial blood gas (ABG) measurement. In addition, urinary catheters can be placed to monitor urine output and assess for hematuria. Gastric catheters decompress distention and assess for evidence of blood. Other helpful tests include blood lactate, x-ray examinations (e.g., chest and pelvis), FAST, extended focused assessment with sonography for trauma (eFAST), and DPL.
Cervical spine injury – 1.2-7.8%
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A detailed secondary survey is important because more than half of patients with severe head injury have other major injuries
The secondary survey is a head-to-toe evaluation of the trauma patient—that is, a complete history and physical examination, including reassessment of all vital signs.
Adjunct exams: additional x-ray examinations of the spine and extremities; CT scans of the head, chest, abdomen, and spine; contrast urography and angiography; transesophageal ultrasound; bronchoscopy; esophagoscopy; and other diagnostic procedures
CT has become the primary neuroimaging technique in the assessment of TBI because of its rapid acquisition time, global availability in developed countries, easy interpretation, and reli- ability
ATLS guidelines suggest a goal of 30 minutes between initial assessment and CT scan.
The Canadian CT Head Rule is a well-validated clinical decision aid that allows physicians to safely rule out the presence of intracranial injuries that would require neurosurgical intervention without the need for CT imaging
Five high risk factors and two medium risk factors were identified to predict the need for subsequent neurosurgical intervention
Five high risk factors and two medium risk factors were identified to predict the need for subsequent neurosurgical intervention
High-Risk Factors • Failure to reach GCS score of 15 within 2 hours • Suspected open skull fracture • Any sign of basal skull fracture (e.g., Battle’s sign, periorbital ecchymosis, cranial nerve palsy, hemotympanum)
• More than two episodes of vomiting • Age older than 65 years
Medium-Risk Factors • Amnesia after impact for longer than 30 minutes
• Dangerous mechanism of injury
If the patient does not have any of the risk factors identified by the CCTHR then the CT head is deemed unnecessary.
If any of the above risk factors are identified then a CT head should be obtained.
Why 30 degrees? No kinking of IJV
Decreased incidence of VAP
Peak sacral interface pressures increased with large increases in head of bed elevation.
Raising the head of bed to 30 degrees or higher on a intensive care unit bed increases the peak interface pressure between the skin at the sacral area and support surface in healthy volunteers.
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Peak sacral interface pressures increased with large increases in head of bed elevation. The 30 degrees , 45 degrees , 60 degrees , and 75 degrees head of bed positions all had peak interface pressures that were significantly (p < 0.02) greater than the supine measurement and also were different from all other head of bed positions. Affected areas, defined as areas over which an interface pressure >or=32 mm Hg was obtained, increased with large elevation of the head of bed. The affected areas of the 45 degrees , 60 degrees , and 75 degrees head of bed positions were significantly greater than the supine position and were also significantly different from all other head of bed positions.
Goals: Restore organ perfusion and tissue oxygenation
*this may decrease mortality and improve outcomes (Class III)
(scalp lac massive exsanguination)
Patient with severe TBI require definitive airwary protection because they are at risk of pulmonary aspiration and compromised respiratory drive and function
Under normal conditions, PaCO2 is the most powerful determinant of CBF and between a range of 20-80mmHg, CBF is linearly responsive to PaCO2
Use hyperventilation only in moderation and for as limited a period as possible. In general, it is preferable to keep the PaCO2 at approximately 35 mm Hg (4.7 kPa), the low end of the normal range (35 mm Hg to 45 mm Hg).
Vasoconstrict ischemia
The BTFG Committee is universal in it belief that hyperosmolar agents are useful in the care of patients with TBI
Mannitol is an osmotic diuretic that decreases water and sodium reabsorption in the renal tubule
Rheological effect (by reducing blood viscosity), promotes plasma expansion and cerebral oxygen delivery in response, there is cerebral vasoconstriction decreasing CBF
Creates an osmotoic gradient across the BBB movement of water from the parenchyma to the intravascular space brain tissue volume decreased ICP lowered
Osmotic diuretic free water clearance and increase in serum osmolality (water moves from intracellular to extracellular space)
Acute neurological deterioration— such as when a patient under observation develops a dilated pupil, has hemiparesis, or loses consciousness—is a strong indication for administer- ing mannitol in a euvolemic patient. In this case, give the patient a bolus of mannitol (1 g/ kg) rapidly (over 5 minutes) and transport her or him immediately to the CT scanner—or directly to the operating room,
BOLUS DOSE OF HTS:
Emergent Intracranial Process • Acute intracranial hypertension defined as sustained elevation in ICP>22mmHg • Known intracerebral lesion (e.g.hemorrhage/mass/cerebraledema) with signs/symptoms of impending cerebral herniation
• Acute cerebral edema defined as evidence new/worsening cerebral edema on brain imaging.
In patients with severe hyponatremia, serum sodium should undergo correction by 4 to 6 mEq/L per day, which can be achieved with 100 mL boluses of 3% HS at 10-minute intervals up to three total boluses. Some authorities recommend up to 8 mEq/L per day
HTS more advantageous: morality not significantly different, ICU stays shorter for HTS group
HTS bolus has been shown to be effective in treating increased intra-cranial pressure (ICP) and cerebral edema due to traumatic brain injury, cerebrovascular accident, and aneurysmal hemorrhage.
BOLUS DOSE OF HTS:
Emergent Intracranial Process • Acute intracranial hypertension defined as sustained elevation in ICP>22mmHg • Known intracerebral lesion (e.g.hemorrhage/mass/cerebraledema) with signs/symptoms of impending cerebral herniation
• Acute cerebral edema defined as evidence new/worsening cerebral edema on brain imaging.
In patients with severe hyponatremia, serum sodium should undergo correction by 4 to 6 mEq/L per day, which can be achieved with 100 mL boluses of 3% HS at 10-minute intervals up to three total boluses. Some authorities recommend up to 8 mEq/L per day
Monro-Kellie doctrine states that under normal conditions, the intracranial compartment space, cerebral blood volume, and volume inside the cranium are fixed volumes --> if any of these components increase, then compensation must occur to maintain ICP within normal range
For ICP, the identified threshold was 22mmhg for both mortality and favorable outcome for all patients
18mmHg – favorable outcome for patients >55 and women of all ages
Recommended CPP for survival and favorable outcomes is 60-70mmHg
Higher than 70 risk of ARF
**why don’t we use ICP monitors anymore? no difference in 6month mortality monitor vs clinical
What are the indications for ICP monitoring
Severe TBI pts
CMRO2 – cerebral metabolic rate of oxygen
CBF – blood flow
Inhibit O2 radical mediated lipid peroxidation
Precedex dose: continuous infusion is 0.2 to 0.7 μg/hr for 24 hour
Barbiturate coma burst suppression via EEG as prophylaxis NOT recommended
Ensure hemodynamic instability
Propofol not recommended as high doses significant morbidity
Propofol has the advantage of a short half-life, which allows intermittent neurological examination, but is a potent systemic vasodilator and can cause hypotension that exceeds the reduction in ICP so that CPP can be significantly reduced.186 Propofol infusion syndrome can result as a conse- quence of the use of high doses of propofol. Some clinical features are hyperkalemia, hepatomegaly, lipemia, metabolic acidosis, myocardial failure, rhabdomyolysis, and renal failure.
Propofol is not recommended for improvement in mortality or 6-month outcomes.
Side effects include hypotension, decreased cardiac output --> hypoxia decrease CPP
•Nutritional support given within 5 days associated with significant decrease in mortality
•catabolic phase, decrease in protein decrease in effectivity of medical decompression
•mod-to-sev tbi, can need as much as 1.5 grams protein/kg/day
•early alimentation may improve endo factors (TSH, FT4, FT3)
•Early feeding protective, lower rates of EVAP
•intragastric feeding residual, delayed gastric emptying and aspiration pneumonia
•Feeding intolerance greater in bolus group, continuous group reached 75% of nutrition goal earlier, trend towards less infection
• Enteral feedings are preferable to parenteral feedings because gut integrity is better maintained, and this may reduce the risk of sepsis.
• Endoscopic evidence of mucosal damage can appear within 24 hours of a severe brain injury, and 17% of these early erosions can progress to clinically significant hemorrhage
*early trache no evidence decreases mortality or pneumonia but reduces MV days and decreases ICU stay
Risk factors: GCS <10, immediate seizures, amnesia >30mins, linear or depressed skull fracture, age <65, chronic alcoholism, intracranial bleeds (EDH, SDH, contusions, ICH)
Although seizures can dramatically increase cerebral metabolic rate, there is not a clear relationship between the occurrence of early seizures and a worse neurological outcome
12hrs, 24hrs
12hrs, 24hrs
Add DAI
The histologic findings of DAI have been well described and include disruption and swelling of axons, “retraction balls” (swollen proximal ends of severed axons), and punctate hemor- rhages in the pons, midbrain, and corpus callosum.
Strich hemorrhages, that represent bleeding from small cerebral vessels.141 Strich hemorrhages are typically found in areas that experience maximal acceleration forces during trauma: corpus callosum, peri-third ventricular structures (hypothalamus, columns of the fornix, anterior commissure), internal capsule, basal ganglia, dorsolateral brainstem, and superior cerebellar peduncles.
A definitive diagnosis of diffuse axonal injury can be made in the postmortem pathologic examination of brain tissue. However, in clinical practice, a diagnosis of diffuse axonal injury is made by implementing clinical information and radiographic findings
Generally, DAI is diagnosed after a traumatic brain injury with GCS less than 8 for more than six consecutive hours.
Strich hemorrhages, that represent bleeding from small cerebral vessels.141 Strich hemorrhages are typically found in areas that experience maximal acceleration forces during trauma: corpus callosum, peri-third ventricular structures (hypothalamus, columns of the fornix, anterior commissure), internal capsule, basal ganglia, dorsolateral brainstem, and superior cerebellar peduncles.
Overall, CT head has a low yield in detecting diffuse axonal injury-related injuries.
Multiple hemorrhagic lesions are seen in gray white matter junction of bilateral cerebral hemispheres. The larger lesions are surrounded by significant edema.
Currently, magnetic resonance imaging (MRI), specifically diffuse tensor imaging (DTI), is the imaging modality of choice for the diagnosis of diffuse axonal injury.
Strich hemorrhages, that represent bleeding from small cerebral vessels.141 Strich hemorrhages are typically found in areas that experience maximal acceleration forces during trauma: corpus callosum, peri-third ventricular structures (hypothalamus, columns of the fornix, anterior commissure), internal capsule, basal ganglia, dorsolateral brainstem, and superior cerebellar peduncles.
