TRAUMATIC BRAIN INJURY
PRESENTER :GEORVIN MARCO
SUPERVISOR:Dr.LIMERI
Learning objectives
• At the end of session we must be able to
• Define traumatic brain injury .
• Classify traumatic brain injury .
• Explain the pathophysiology of traumatic brain
injury .
• Evaluate and explain management of patient
with traumatic brain injury.
• Explain pathophysiology and management of
raised intracranial pressure.
Outline
• Introduction
• Classification of traumatic brain injury
• Type of primary brain injury
• Pathophysiology of Secondary traumatic brain
injury
• Pathophysiology and management of raised
intra cranial pressure.
• Management of traumatic brain injury.
Introduction
• is an alteration in brain function, or other evidence of brain
pathology, caused by an external force
• the presence of confounding factors such as intoxication or
medical illness does not preclude a diagnosis of TBI,
• although clinical judgment is used to decide whether the
patient's symptoms are a consequence of the TBI.
• clinical symptoms of brain injury may be delayed or absent,
and that "other evidence of brain pathology" can include
imaging or laboratory investigations.
Epidemiology
• Traumatic brain injury (TBI) has been one of the leading causes
of morbidity, disability and mortality across all ages Globally.
• More than 50 million individuals suffer from TBIs each year
• Approximately 3.17 million TBI survivors experience post-
traumatic complications ranging from neurological,
psychosocial problems to long-term disability
• The immense expenditure on clinical management of TBI
patients and associated socioeconomic problems have
imposed a heavy burden on the healthcare system and the
society .
Classification
• TBI is not as single disease (heterogeneous)
There are many different ways to categorize
patients in terms of
• clinical severity, mechanism of injury, and
pathophysiology,
• from above classification , each may impact
the prognosis and treatment.
Classification according to mechanism
• unique physical mechanisms of insult, TBI can be
divided into three categories:
• (i) closed head
• (ii) penetrating and
• (iii) explosive blast TBI.
• E xternal forces may be, head being struck by an
object,head striking an object,
• Acceleration/deceleration of the brain without direct
external impact,A foreign body penetrating the brain
the force from a blast/explosive
Classification by clinical severity score
• TBI has traditionally been classified using
injury severity scores; the most commonly
used is the Glasgow Coma Scale (GCS) ,
• A GCS score of 13 to 15 is considered mild tb
injury,
• 9 to 12 is considered moderate tb injury,
• and 8 or less is considered severe TBI.
GSC –Pupil score
Unresponsive patient (FOUR SCORE)
• For patient who are intocated , intubated and
all unreponsive patient
Classification by neuroimaginging score
• tbi lead to several pathologic injuries, most of which can be identified on
neuroimaging,
• Two currently used computed tomography (CT)-based grading scales are
the Marshall scale and the Rotterdam scale:
• The Marshall scale uses CT findings to classify injuries in six ,has been
shown to predict the risk of increased intracranial pressure (ICP) and
outcome in adults accurately, but lacks reproducibility in patients with
multiple types of brain injury.
• The Rotterdam scale is a more recent CT-based classification developed to
overcome the limitations of the Marshall scale It has shown promising
early results but requires broader validation .
Clinical presentation of TBI
• Clinical features of TBI include prolonged coma, headache,
nausea, aphasia, seizures, amnesia and behavioral
abnormalities such as aggression and anxiety, which occur
within seconds to minutes after TBI
• however, some of these manifestations can persist up to
months and years.
Pathophysiology of TBI
• Damages of neuronal tissues associated with TBI fall into two
categories:
• (i) primary injury, which is directly caused by mechanical
forces during the initial insult; and
• (ii) secondary injury, which refers to further tissue and
cellular damages following primary insult.
Pathophysiology of TBI
• The Monro-Kellie hypothesis states that
• the total intracranial volume (composed of brain tissue,
cerebrospinal fluid, venous blood, and arterial blood) should
always remain a constant since the cranium is a rigid and non-
expansile container.
• When an additional compartment is introduced (like a
hematoma), there must be a compensatory reduction in another
compartment in order to prevent intracranial hypertension.
• CPP= MAP-ICP.
• The goal of TBI management is to prevent this secondary insult
Pathophysiology of TBI
• Primary brain injury occurs at the time of trauma. Common
mechanisms include direct impact, rapid
acceleration/deceleration, penetrating injury, and blast waves.
• Although these mechanisms are heterogeneous, they all result
from external mechanical forces transferred to intracranial
contents.
• The damage that results includes a combination of focal
contusions and hematomas, as well as shearing of white matter
tracts (diffuse axonal injury [DAI]) along with focal and global
cerebral edema.
Concussion
• This is usually a mild TBI without any gross structural damage
and occurs secondary to a nonpenetrating TBI.
• It usually results from acceleration/deceleration forces
occurring secondary to a direct blow to the head.
• It causes a transient altered mental status, which can range
from confusion to loss of consciousness.
• This cannot be diagnosed with a routine computed tomogram
(CT) scan or magnetic resonance imaging (MRI) scan. Special
sequence MRI like diffusion tensor imaging and functional
MRI may result in earlier diagnosis of concussion.
EPIDURAL HEMATOMA
• An epidural hematoma (EDH) typically occurs at the site of
traumatic impact or “coup” site and is almost always
associated with an overlying skull fracture.
• EDHs are most common in the temporal or temporo-parietal
regions, often due to laceration of the middle meningeal artery
or one of its branches.
• On imaging, EDHs typically appear lentiform or biconvex in
shape and do not cross cranial sutures because the periosteal
layer of the dura adheres tightly to the suture.
Epidural cont..
• However, unlike subdural hematomas, EDHs can cross the
midline where the periosteal layer of the dura forms the outer
wall of the superior sagittal sinus, which may be displaced from
the inner table of the skull.
• Also, unlike subdural hematomas, EDHs can extend above and
below the tentorium cerebelli, which is a dural reflection
separating the cerebellum from the occipital lobes.
SUBDURAL HEMORRAGE
• A subdural hematoma (SDH) can occur either at the coup
or contrecoup site, although the latter is more common.
Injury to superficial bridging veins results in bleeding
between the meningeal layer of the dura and arachnoid,
• blood may continue to accumulate in this space as
bridging veins are progressively stretched and injured.
• SDHs commonly occur over the cerebral convexities,
along the tentorium cerebelli, and along the falx cerebri,
in descending order of frequency
• On imaging, SDHs appear crescentic in shape and do not cross
the midline; they can, however, cross cranial suture lines
(unlike EDHs).
• Most SDHs in the setting of acute TBI are homogeneously
hyperintense on noncontrast CT scans.
SUBARACHNOID HEMORRAGE
• Subarachnoid hemorrhage (SAH) occurs in ~40% of patients
with moderate to severe head injury and is commonly
associated with other types of intracranial hemorrhage.
• Patients with traumatic SAH have a significantly worse
outcome than those without SAH: 41% of patients without
traumatic SAH achieved a level of good recovery compared
with only 15% of patients with SAH, according to the results
of a large study conducted by the European Brain Injury
Consortium.
• Hydrocephalus is a common complication of traumatic SAH
and may develop acutely or in a delayed fashion.
• Intraventricular hemorrhage or inflammatory arachnoiditis
may result in hydrocephalus in the acute setting, while
decreased resorption of CSF by arachnoid villi is responsible
for chronic hydrocephalus
CORTICAL CONTUSIONS/HEMATOMA
• Cortical contusions in closed head injury result when the brain is
bruised by the irregular inner surfaces of the skull at the time of
impact.
• They can occur at the coup site when a depressed skull fracture
or transient calvarial deformity from a blow to the stationary
head grazes the underlying cortex.
• More commonly, however, they occur at the contrecoup location
when the moving head collides against a stationary object. These
contrecoup contusions are frequently of greater severity than the
injuries at the coup site.
Intracerebral hematoma
• Occur within the cerebral parenchyma secondary to
lacerations or contusion of the brain, with injury to larger,
deeper cerebral vessels occurring with extensive cortical
contusion.
• The specific indications for craniotomy and surgical evacuation in
patients with contusion or ICH have not been established.
• Generally, a combination of clinical and radiologic factors is felt to
be important, including hemorrhage location and volume, extent of
mass effect on CT (cisternal effacement or midline shift), GCS
score, ICP, and neurological deterioration.
• Patients with contusions/ICH and progressive neurological decline,
medically refractory increased ICP, or radiographic evidence of
mass effect tend to have poor outcome without surgical treatment,
although specific surgical criteria have not been established.
TRAUMATIC AXONAL INJURY
• Traumatic axonal injury (TAI) is also commonly referred to as
diffuse axonal injury or shear injury. The term TAI is preferred
by the authors of this review as injuries are not distributed
diffusely throughout the whole brain, but occur in characteristic,
discrete locations, including the parasagittal white matter near
the cerebral cortex, corpus callosum, and brainstem.
• Mild (grade I) TAI involves the gray–white junction of the lobar
white matter, particularly the parasagittal frontal lobes;
• moderate (grade II) TAI involves the fibers of the corpus
callosum, particularly the splenium, in addition to the
subcortical white matter;
• severe (grade III) TAI involves the dorsolateral midbrain, in
addition to the subcortical white matter and corpus callosum
• The mechanism of injury is one of cytoplasmic shear-strain of
the axonal cytoskeleton due to sustained
acceleration/deceleration, such as that which occurs with a
high-speed motor vehicle crash or prolonged shaking.
• Damage to the neurons occurs not only at the time of
mechanical injury but in the hours, days, and weeks, even
years, following the traumatic event due to a deleterious
cascade of biochemical events and Wallerian-type
degeneration with progressive neuronal loss
Secondary Injury
– Primary injury →Impaired autoregulation of CBF and metabolism
→Ischemia →anaerobic glycolysis leading to:-
• Accumulation of lactic acid
• ↑Membrane permeability
• Edema formation
Pathophysiology is predominantly derived from
• Cerebral blood flow
• Cerebrovascular autoregulation and co2 reactivity
• Cerebral vasospasm
• Cerebral metabolism dysfunction
• Excitotoxicity and oxidative stress
• Cerebral oxygenation
• Oedema
• Inflammation
treatment for Mild TBI
• Bed rest, elevate head of bed 30-45º
• Serial neural exams.
• Isotonic IVF e.g N/S
• Mild analgesics (PCM, Codeine)
• Enteral feeding
treatment for moderate TBI
• Admit to ICU if CT shows significant
abnormality
• Pts with normal CT should improve, if not
repeat CT.
treatment protocol for severe tbi
• Maintain airway, intubation • Sedation for agitation
Breathing SPO2≥90% • GI ulcer prophylaxis
• SBP≥90mmhg
• Keep Temp ≤ 37.5
• Maintain c spine stability
• Insert ICP monitor/evd • Feeding NGT
• Continuous cardiac • DVT prophylaxis
monitoring • Monitor rbg,
• Elevate head at 30-45
electrolytes
• Maintain CPP 60-80mmHg
• Mannitol
• Hypertonic saline
• Intubation
– Indications
• GCS < 8
• Need for Hyperventilation
• Severe maxillofacial trauma
• Need for pharmacological paralysis
• Hyperventilation
– Reserved for
• Herniating patients or progressive
neurologic deteriorating patients
– Ventilate to pCO2 < 30-35mmHg
– Acute alkalosis increase protein- bind of
Calcium ↓Ca++ causing hypocalcemic tetany
mannitol
• Early use of Mannitol
– Use before ICP monitoring is reserved for
» Patient who are euvolemic with signs of
transtentorial herniation
– Indications:- evidence of IC-HTN, mass effect,
sudden deterioration prior to CT Scan.
To asses salvageability in pts with no evidence of brain
function
– Contraindications:- Prophylaxis, hypotension, CHF
• Administration: bolus 0.25-1gm/kg <20min (350mls)
ICP monitoring
• Indications
• GCS ≤ 8 and either abnormal admitting CT or ≥2 risk
factors for IC-HTN
• Polytrauma patient with altered level of consciousness
(Heavy sedation)
• Traumatic intracranial mass
• Contraindications
• Awake patient who can follow neural exam
• Coagulopathy
• Duration of monitoring
– Discontinue when ICP is normal 48-72hrs after
stopping ICP therapy
– NB: caution delayed onset (2-3 and 9-11days.
Complications: Infection, Haemmorrhage,
malposition or malfunction
• Types of ICP monitors
1. Intraventricular catheter (IVC) a.k.a EVD connected to
external pressure transducer via fluid filled tubing
2. Intraparenchymal monitor
3. Less accurate monitors
1. Subarachnoid screw
2. Subdural:use fluid coupled/fibreoptic catheter
3. Epidural :use fluid coupled/fibreoptic catheter
4. Open anterior fontanelle in infants
Conversion: 1mmHg(torr)=1.36cmH2O
ICP treatment measures
• Initiated when ICP is 20-25mmHg
• CPP should be maintained ≥ 70mmHg
General measures
1) Elevate HOB to 30-45º
2) Keep neck straight and avoid tight bandaging
3) Avoid Hypotension (SBP<90mmHg)
4) Control HTN if present
5) Avoid Hypoxia (pO2<60mmHg)
6) Ventilate to normocarbia (35-40mmHg)
7) Light sedation: codeine 30-60mg IM4hrly PRN
8) Unenhanced head CT scan for ICP problems
Specific measures for IC-HTN
1) Heavy sedation (MgSO4 2-4mg IV hrly,or fentanyl1-2mls and
paralysis (Vecuronium 8-10mg IV)
2) Drain 3-5ml of CSF if IVC present
3) Mannitol if no hypovolemia or hypotension.
(0.25-1g/kg start then 0.25g/kg 6hrly.↑dose if IC-HTN persist and Osm
≤320) /Hypertonic saline
4) Hyperventilate to pCO2=30-35mmHg
If ICP still refractory → Decompressive craniectomy
.
• Exploratory Burr holes
– Indications
• Deteriorating neurological exam
– Sudden drop in GCS
– One pupil dilates and fixes
– Paralysis or decerebrate
• Pts with other major injuries who cannot wait for CT
.
• Decompressive craniectomy
– Can be done in two different situations
a. Prophylactic or primary decompression
b. Therapeutic or secondary decompression
• Prophylactic/primary decompressive
craniectomy
– is defined as any surgical decompression performed, with or without brain tissue
removal, in patients undergoing surgery primarily for the evacuation of any type
of intradural lesion.
– Aim is to avoid expected postsurgical increases in
ICP
• Therapeutic/secondary craniectomy
– procedure performed in patients in whom
continuous ICP monitoring is conducted and in
whom high ICP is refractory to medical treatment
– used in some centers after first- or second-line
therapeutic measures have failed to control ICP
– the purpose of surgical decompression is to
control high ICP
Summary
● Management of head injuries requires
an understanding of basic intracranial
physiology.
● Efficient evaluation of head and brain
injuries includes ABCs, a neurologic
examination and searching for
associated injuries.
● Adequate resuscitation is important in
limiting secondary brain injury.
THANK YOU
References
• Ng, S. Y., & Lee, A. Y. (2019). Traumatic Brain Injuries:
Pathophysiology and Potential Therapeutic Targets.
Frontiers in Cellular Neuroscience, 13.
https://doi.org/10.3389/fncel.2019.00528
• Uptodate
• Munakomi S, M Das J. Brain Herniation. [Updated
2023 Mar 13]. In: StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2023 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK542246/
