TBI CME for postgraduate students teaching

MedicNerd 23 views 55 slides Mar 06, 2025
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About This Presentation

TBI is improtant subject must know for PG students


Slide Content

PRESENTER : DR JOANNE QUAY
SUPERVISOR : PROF. DATO’
DR MOHD BASRI MAT NOR
1

OUTLINE
•INTRODUCTION
•DEFINITION OF TBI
•CLASSIFICATIONS OF TBI
•PATHOPHYSIOLOGY
•ICU MANAGEMENT
2

INTRODUCTION
•Traumatic brain injury (TBI) is a leading cause of death and disability worldwide
•Many survivors live with significant disabilities resulting in major socioeconomic
burden and a greater economic toll.
•In Malaysia, TBI was deemed as one of the top 3 common admissions reported in
ICU
•National Trauma Database Malaysia 2009 reported - 80% of traumas were caused by
road traffic accidents
•64% of these cases - related to TBI.
3

DEFINITION
•Traumatic brain injury (TBI) is an alteration in brain function, or other
evidence of brain pathology, caused by an external force
•Outcome of severe TBI ~ 30% risk of death, 5-15% discharged in
vegetative state.
•Moderate TBI ~ 15% mortality, only 20% back to functioning baseline
•Patients in specialized neuro- intensive care units with guideline-driven
protocols are associated with better outcomes
4

CLASSIFICATION OF TBI
The severity of TBI according to
the GCS score (within 48 h):
Mild TBI = 14-15
Moderate TBI = 9-13
Severe TBI = <9
*Confounding factors:
- Drugs/intoxication
- Other Injuries
- Hearing impairment
- Intubation
- Language barrier
- Underlying mental impairment
5

CLASSIFICATION OF TBI
Full Outline of UnResponsiveness(FOUR) Score
A. EYE RESPONSE
4 eyelids open or opened, tracking, or blinking to
command
3 eyelids open but not tracking
2 eyelids closed but open to loud voice
1 eyelids closed but open to pain
0 eyelids remain closed with pain
B. MOTOR RESPONSE
4 thumbs-up, fist, or peace sign
3 localizing to pain
2 flexion response to pain
1 extension response to pain
0 no response to pain or generalized myoclonus status
6

C. BRAINSTEM REFLEXES
•4 pupil and corneal reflexes present
•3 one pupil wide and fixed
•2 pupil or corneal reflexes absent
•1 pupil and corneal reflexes absent
•0 absent pupil, corneal, and cough reflex

D. RESPIRATION
•4 not intubated, regular breathing pattern
•3 not intubated, Cheyne–Stokes breathing
pattern
•2 not intubated, irregular breathing
•1 breathes above ventilator rate
•0 breathes at ventilator rate or apnea
7

CLASSIFICATION OF TBI
NEUROIMAGING
The Marshall scale
8

CLASSIFICATION OF TBI
The Rotterdam scale
Prognosis
Mortality at 6 months increases
with the score:
•score 1: 0%
•score 2: 7%
•score 3: 16%
•score 4: 26%
•score 5: 53%
•score 6: 61% 9

PATHOPHYSIOLOGY
PRIMARY BRAIN
INJURY
SECONDARY BRAIN
INJURY
10

PATHOPHYSIOLOGY
Primary Injury
CT scan showing
DAI. Deep
shearing-type
injury near the
white matter of
the left internal
capsule
CT scan
depicting
cerebral
contusions at
basal frontal
areas 11

12

PATHOPHYSIOLOGY
Secondary Injury
13

Physiological and Cellular Changes Associated Secondary Brain Injury
• - Primary injury exhausts the compensatory capacity of the brain
- Leads to increase in ICP (Monroe - Kelly doctrine)
- Results in cerebral ischemia and hypoxia
•Inflammation and local tissue damage cause excessive release of
excitatory neurotransmitters, resulting in calcium influx to cells, cell
edema and death
14

•Dying cells release mediators (platlet activating factor, leukotrienes, o2
free radicals) --> affecting blood vessel permeability--> vasogenic fluid
accumulation --> increasing ICP --> hypoperfusion, cerebral ischemia
and neurodegeneration
•These can lead to neuronal cell death as well as to cerebral edema and
increased ICP that can further exacerbate the brain injury.
•Critical aspect of ameliorating secondary brain injury after TBI is the
avoidance of secondary brain insults
15

16

17

EXTRACRANIAL COMPLICATIONS
18

Acute Management of TBI
•Prehospital management for moderate and severe TBI is prevention and
treatment of hypotension and hypoxia
•The injured brain is especially vulnerable to secondary insults in the first
24 hours.
•Hypoxia (PaO2<60 mmHg) and Hypotension (SBP <90 mmHg) were
present in 50 and 30 % of patients
•Associated with a higher likelihood of a poor outcome
19

20

WHEN TO DO CT BRAIN ?
21

INDICATION FOR SURGERY
•Epidural hematoma– Surgical guidelines recommend evacuation of an
epidural hematoma (EDH) larger than 30 mL in volume regardless of a
patient's GCS score
•Subdural hematoma– Acute subdural hematomas (SDHs) >10 mm in
thickness or associated with midline shift >5 mm
•Intracerebral hemorrhage– Surgical evacuation of a traumatic
intracerebral hemorrhage (ICH) in the posterior fossa when there is
evidence of significant mass effect
•Depressed skull fracture– Elevation and debridement for open skull
fractures depressed greater than the thickness of the cranium or if there
is dural penetration, significant intracranial hematoma, frontal sinus
involvement 22

23

ICU MANAGEMENT
24

Treatments
Decompressive Craniectomy
Prophylactic Hypothermia
Hyperosmolar Theraphy
Cebebrospinal Fluid Drainage
Ventilation Theraphies
Anaesthetics, Analgesics and Sedatives
Steroids
Nutrition
Infection Prophylaxis
Deep Vein Thrombosis Prophylaxis
Seizure Prophylaxis
Monitoring
Intracranial Presue
Cerebral Perfusion Pressure
Advanced Cerebral Monitoring
Thresholds
Blood Pressure
Intracranial Pressure
Cerebral Perfusion Pressure
Advanced Cerebral Monitoring
25

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27

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30

WHEN IS ICP MONITORING INDICATED?
31

ICP MONITORING
4 main anatomic sites used in
the clinical measurement of
ICP:
• Intraventricular
• Intraparenchymal
• Subarachnoid
• Epidural
32

METHODS ADVANTAGES DISADVANTAGES
External Ventricular Drainage Gold standard
Accurate
Simple measurement
Allow treatment of some
cause of elevated ICP
Infection – 20% of patient
Hemorrhage during
placement
Intraparenchymal Ease of placement
Lower risk of infection and
hemorrhage - <1%
Inability to drain CSF
Greater risk of mechanical
failure due to complexity
Subarachnoid Less invasive
Lower risk of infection and
hemorrhage
Clog with debris cause
unreliable measurement
Less accurate
Epidural Used in management of
coagulopathic patients with
hepatic encephalopathy
complicated with cerebral
edema
Low risk of intracerebral
Hemorrhage
Inaccurate
33

ICP MONITORING AND WAVE INTERPRETATION
34

35

ADMISSION AND INITIAL MANAGEMENT
36

37

38

Background: Current guidelines for the treatment of adult severe traumatic brain injury (sTBI) consist of
high-quality evidence reports, but not accompanied by management protocols
Results: established three distinct treatment protocols, each with three tiers whereby higher tiers involve
therapies with higher risk
39

MANAGEMENT OF SEVERE TBI GUIDED BY
INTRACRANIAL PRESSURE AND BRAIN TISSUE
OXYGEN
A combination of the two parameters
creates a matrix of four potential clinical
conditions
No Level I evidence that supports the use
of brain tissue oxygen monitoring, the
phase II BOOST2 trial demonstrated that
a protocol guided by ICP and PbtO2
could reduce brain hypoxia
40

41

SUMMARY
Recommendation Justification
Blood pressure SBP ≥100 mmHg- patients 50 to 69 years old
≥110 mmHg for patients 15 to 49 or >70 years old
Cerebral perfusion pressure CPP of 60 to 70 mmHg
ICP < 22 mmHg
Ventilation PaO
2 >60 mmHg
Avoid PaCO
2 <30 mmHg
Temperature management Avoid temperature > 38 °C
Antiseizure medication Prophylactic AEDs for 1 week
42

SUMMARY
Recommendation Justification
Glucose management Blood sugar 6-10.0 mmol/L
Nutritional support Establish early enteral feeding within 5-7 days

Sedation and analgesia RASS of -4 to -5 , when ICP elevated
RASS of 0 to -2 when ICP controlled
Glucocorticoids Harmful according to CRASH trial

ICP and CPP monitoring ICP should be monitored in all salvageable patients
with a severe TBI and abnormal CT scan
43

•CRASH 3 trial- the use of tranexamic acid in TBI patients with GCS <13 or with any
intracranial bleeding on CT within 3 hours of injury.
•Reduction in the risk of head injury-related death in patients treated with tranexamic
acid, which almost reached statistical significance.
•Administration of 1 gram of tranexamic acid as a bolus, followed by 1 gram of tranexamic
acid infused over 8 hours
44

FLUID SELECTION
SAFE TRIAL
45

PROPHYLACTIC HYPOTHERMIA
POLAR and Eurotherm3235 Study
46

DECOMPRESSIVE CRANIECTOMY
Conclusion from DECRA and RESCUEicp :
Decompressive craniectomy for patients with traumatic brain injury improved survival, while increasing the
likelihood of poor neurological outcomes.
RESCUEicp
DECRA
47

REFERENCES
•Hawryluk, Gregory W J et al. “A management algorithm for patients with intracranial
pressure monitoring: the Seattle International Severe Traumatic Brain Injury
ConsensusConference (SIBICC).” Intensive care medicine vol. 45,12 (2019): 1783-
1794.doi:10.1007/s00134-019-05805-9
•Chesnut, Randall et al. “A management algorithm for adult patients with both brain
oxygen and intracranial pressure monitoring: the Seattle International Severe
Traumatic Brain Injury Consensus Conference (SIBICC)
•UpToDate - Traumatic brain injury: Epidemiology, classification, and pathophysiology
•UpToDate - Management of acute moderate and severe traumatic brain injury
•UpToDate – Anesthesia for patients with acute traumatic brain injury
•UpToDate – Evaluation and management of elevated intracranial pressure in adults
•BTF. Guidelines for the Management of Severe Traumatic Brain Injury.4th Ed. 2016
48

SBA
A 27-year-old man is admitted with a severe traumatic brain injury following
a road-traffic collision. He has sustained a large subdural haematoma and
undergoes prompt surgical evacuation. Post-operatively, he is transferred,
intubated and sedated to the intensive care unit, with an intracranial pressure
monitor inserted.
Which of the following is most likely to be associated with an improved clinical
outcome from traumatic brain injury?
A. A cerebral perfusion pressure of greater than 75 mmHg
B. Induced hypothermia
C. High-dose steroids
D. Prophylactic thiopentone infusion
E. Normoglycaemia
49

SBA
A 27-year-old man is admitted with a severe traumatic brain injury following
a road-traffic collision. He has sustained a large subdural haematoma and
undergoes prompt surgical evacuation. Post-operatively, he is transferred,
intubated and sedated to the intensive care unit, with an intracranial pressure
monitor inserted.
Which of the following is most likely to be associated with an improved clinical
outcome from traumatic brain injury?
A. A cerebral perfusion pressure of greater than 75 mmHg
B. Induced hypothermia
C. High-dose steroids
D. Prophylactic thiopentone infusion
E. Normoglycaemia
50

SBA
5 days ago a 25-year-old woman suffered a traumatic brain injury. Despite a
normal CT, she demonstrated bilateral motor posturing. She therefore had an
intracranial pressure (ICP) bolt inserted shortly after admission in order to
monitor her ICP. You begin your morning review by analysing her ICP waveform.
Which of the following would concern you most acutely?
A Lundberg A waves
B A flat trace
C A baseline value of 20mmHg
D Lundberg B waves
E The most prominent upstroke being the P2 (tidal) wave
51

SBA
5 days ago a 25-year-old woman su!ered a traumatic brain injury. Despite a
normal CT, she demonstrated bilateral motor posturing. She therefore had an
intracranial pressure (ICP) bolt inserted shortly after admission in order to
monitor her ICP. You begin your morning review by analysing her ICP waveform.
Which of the following would concern you most acutely?
A Lundberg A waves
B A flat trace
C A baseline value of 20mmHg
D Lundberg B waves
E The most prominent upstroke being the P2 (tidal) wave
52

SBA
A 26-year-old gentleman is admitted to the emergency department with a closed traumatic
brain injury following a road traffic collision. On application of a painful central stimulus, his
eyes remain closed, he extends his left arm and he makes incomprehensible sounds.
Computed tomography (CT) of the head reveals a large left-sided fronto-parietal contusion
with obvious midline shift.
Which of the following would be the most appropriate initial interventions, after intubation
and ventilation?
A. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg,
and active cooling to a core temperature of 34 °C
B. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), insertion of an intracranial pressure monitor
and maintenance of a cerebral perfusion pressure of 60 mmHg
C. Aim for a PaCO2 of 4.5 kPa (33.7mmHg) and maintenance of a mean arterial pressure of 100 mmHg
D. Aim for a PaCO2 of 4.0 kPa (30mmHg) and maintenance of a mean arterial pressure of 80 mmHg
E. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg
and administration of high-dose intravenous methylprednisolone
53

SBA
A 26-year-old gentleman is admitted to the emergency department with a closed traumatic
brain injury following a road traffic collision. On application of a painful central stimulus, his
eyes remain closed, he extends his left arm and he makes incomprehensible sounds.
Computed tomography (CT) of the head reveals a large left-sided fronto-parietal contusion
with obvious midline shift.
Which of the following would be the most appropriate initial interventions, after intubation
and ventilation?
A. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg,
and active cooling to a core temperature of 34 °C
B. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), insertion of an intracranial pressure monitor
and maintenance of a cerebral perfusion pressure of 60 mmHg
C. Aim for a PaCO2 of 4.5 kPa (33.7mmHg) and maintenance of a mean arterial pressure of 100 mmHg
D. Aim for a PaCO2 of 4.0 kPa (30mmHg) and maintenance of a mean arterial pressure of 80 mmHg
E. Aim for a PaCO2 of 4.5 kPa (33.7mmHg), maintenance of a mean arterial pressure of 80 mmHg
and administration of high-dose intravenous methylprednisolone
54

THANK YOU
THANK YOU
55
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