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IX. Symptoms Traumatic Brain Injury
Symptoms vary greatly depending on the severity of the head injury, but
may include any of the following:
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Vomiting
Lethargy
Headache
Confusion
Paralysis
Coma
Loss of consciousness
Dilated pupils
Vision changes (blurred vision or seeing double, not able to tolerate
bright light, loss of eye movement, blindness)
Cerebrospinal fluid (CSF) (which may be clear or blood-tinged) coming
out of the ears or nose
Dizziness and balance problems
Breathing problems
Slow pulse
Slow breathing rate, with an increase in blood pressure
Ringing in the ears, or changes in hearing
Cognitive difficulties
Inappropriate emotional responses
Speech difficulties
Difficulty swallowing
Body numbness or tingling
Loss of bowel control or bladder control
Diagnoses are been taken with: CT scan (CAT scan), X-ray, MRI
(Magnetic Resonance Imaging) Scan, Angiogram, ICP Monitor
(registration intracranial pressure).
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X. Intracranial pressure (ICP) and ICP monitoring
A. Introduction
Intracranial pressure, (ICP), is the pressure exerted by the cranium on
the brain tissue, cerebrospinal fluid (CSF), and the brain's circulating
blood volume. ICP is a dynamic phenomenon constantly fluctuating in
response to activities such as exercise, coughing, straining, arterial
pulsation, and respiratory cycle. ICP is measured in millimeters of
mercury (mmHg) and, at rest, is normally less than 10-15 mmHg.
Changes in ICP are attributed to volume changes in one or more of the
constituents contained in the cranium.
ICP monitoring has been established as an important treatment variable in
severe non-penetrating brain injury, both in terms of prognosis and as a
management variable, with intracranial hypertension clearly being
associated with worse recovery and effective control of elevated ICP
appearing to improve outcome
To understand intracranial pressure, think of the skull as a rigid box.
After brain injury, the skull may become overfilled with swollen brain
tissue, blood, or CSF. The skull will not stretch like skin to deal with
these changes. The skull may become too full and increase the pressure
on the brain tissue. This is called increased intracranial pressure.
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B. Increased Intracranial Pressure (ICP)
a. Definition
- Neurological dysfunction and death in TBI are due to:
a.
b.
c.
d.
the brain injury itself,
prolonged coma with its complications,
infections from open wounds or basilar skull fractures,
hydrocephalus from subarachnoid haemorrhage, and, most
important,
e. Increased intracranial pressure.
- Intracranial is caused by:
a. the added mass of epidural, subdural, and intracranial
haematomas and
b. Cerebral oedema which develops around large contusions,
from diffuse vascular injury, and as a result of HIE.
In infants, the skull can expand to some extent. After the sutures
close, it is rigid. The brain and CSF are not compressible. Any
increase in intracranial mass will first displace CSF into the spinal
subarachnoid space. An increase of intracranial pressure above 4050 mm Hg will collapse brain capillaries resulting in global
ischemia.
ICP-monitor and registration
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Raised intracranial pressure indicates an increase in the normal
brain pressure. This can be due to an increase in cerebrospinal fluid
pressure. It can also be due to increased pressure within brain
matter because of lesions or swelling within the brain matter itself.
An increase intracranial pressure is a severe medical problem. The
pressure itself can be responsible for further damage to the central
nervous system by causing compression of important brain
structures and by restricting blood flow through blood vessels,
which supply the brain.
Many conditions can increase intracranial pressure. Common
causes include:
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subdural haematoma
hydrocephalus
brain tumour
hypertensive brain haemorrhage
intraventricular haemorrhage
meningitis
encephalitis
aneurysm rupture and subarachnoid haemorrhage
status epilepticus
stroke
severe head injury
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Measurement of ICP via intra-parenchymal, fibreoptic catheter
intraventricular catheter, subarachnoid screw/bolt, epidural pressure sensor
C. The Monroe-Kellie Hypothesis
The pressure-volume relationship between ICP, volume of CSF, blood,
and brain tissue, and cerebral perfusion pressure (CPP) is known as the
Monroe-Kellie doctrine or the Monroe-Kellie hypothesis.
The Monroe-Kellie hypothesis states that the cranial compartment is
incompressible, and the volume inside the cranium is a fixed volume.
The cranium and its constituents (blood, CSF, and brain tissue) create a
state of volume equilibrium, such that any increase in volume of one of
the cranial constituents must be compensated by a decrease in volume of
another.
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The principal buffers for increased volumes include both CSF and, to a
lesser extent, blood volume. These buffers respond to increases in
volume of the remaining intracranial constituents. For example, an
increase in lesion volume (e.g. epidural hematoma) will be
compensated by the downward displacement of CSF and venous
blood. These compensatory mechanisms are able to maintain a normal
ICP for any change in volume less than approximatly 100-120 mL.
Monro-Kellie principle - regulation of ICP
Normal ICP = 15mmHg
Raised ICP =/ > 20mmHg
A change in one compartment must be balanced by a change in
another (blood, spinal fluid, brain tissue)
 BRAIN = TISSUE 80-85%
CSF 5-12%
BLOOD 3-7%
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Intra-cranial compensation and his limits
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D. Cerebral perfusion pressure
Cerebral perfusion pressure, or CPP, is the net pressure of blood
flow to the brain. It must be maintained within narrow limits because
too little pressure could cause brain tissue to become ischemic (having
inadequate blood flow), and too much could raise intracranial pressure
(ICP).
CPP can be defined as:  CPP = MAP - ICP
CPP is regulated by two balanced, opposing forces: Mean arterial
pressure or MAP, the arithmetic mean of the body's blood pressure, is
the force that pushes blood into the brain, and intracranial pressure is
the force that keeps it out. Thus raising MAP raises CPP and raising
ICP lowers it (this is one reason that increasing ICP in traumatic brain
injury is potentially deadly). CPP, or MAP minus ICP, is normally
between 70 and 90 mmHg in an adult human, and cannot go below 70
mmHg for a sustained period without causing ischemic brain damage.
Children require pressures of at least 60 mmHg.
CPP autoregulates between 80-100mmHg  CPP <50mmHg loss
autoregulation
Physiological process
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decreased BP - cerebral blood vessels dilate
increased BP - cerebral blood vessels constrict
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increase CO2 - cerebral blood vessels dilate
decrease CO2 - cerebral blood vessels constrict
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decrease O2 - cerebral blood vessels dilate
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increased metabolism fever - increased flow
decreased metabolism sedation- decreased flow
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E. Autoregulation
The brain maintains proper CPP through a process called
autoregulation: to lower pressure, blood vessels in the brain called
arterioles dilate, or widen, creating more room for the blood, and to
raise pressure they constrict, or narrow. Thus, changes in the body's
overall blood pressure do not normally alter cerebral perfusion
pressure drastically.
At their most constricted, blood vessels create a pressure of 150
mmHg, and at their most dilated the pressure is about 60 mmHg.
When pressures are outside the range of 50 to 150 mmHg, the blood
vessels' ability to autoregulate pressure through dilation and
constriction is lost, and cerebral perfusion is determined by blood
pressure alone, a situation called pressure-passive flow. Thus,
hypotension (inadequate blood pressure) in a can result in severe
cerebral ischemia in patients with conditions like brain injury, leading
to a damaging process called the ischemic cascade.
Other factors that can cause loss of autoregulation include free radical
damage, nervous stimulation, and alterations in blood gas content.
Amounts of carbon dioxide and oxygen in the blood affect constriction
and dilation even in the absence of autoregulation: excess carbon
dioxide can dilate blood vessels up to 3.5 times their normal size,
lowering CPP, while high levels of oxygen constrict them. Blood
vessels also dilate in response to low pH.
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Thus, when activity in a given region of the brain is heightened, the
increase in CO2 and H+ concentrations causes cerebral blood vessels to
dilate and deliver more blood to the area to meet the increased
demand. In addition, stimulation of the sympathetic nervous system
raises blood pressure and blocking it lowers pressure.
F. Increased ICP
One of the most damaging aspects of brain trauma and other
conditions, directly correlated with poor outcome, is an elevated
intracranial pressure ICP is very likely to cause severe harm if it goes
past 40 mmHg in an adult. Even intracranial pressures between 25 and
30 mm Hg are usually fatal if prologed, except in children, who can
tolerate higher pressures for longer times. Most commonly due in head
injury to intracranial hematoma or cerebral edema, an increase in
pressure can crush brain tissue, shift brain structures, contribute to
hydrocephalus, cause the brain to herniate, and restrict blood supply to
the brain, leading to an ischemic cascade (Graham and Gennareli,
2000).
G. Pathophysiology
The cranium and the vertebral body, along with the relatively inelastic
dura, form a rigid container, such that the increase in any of its contents
--- brain, blood, or CSF --- will increase the ICP. In addition, any
increase in one of the components must be at the expense of the other
two, a relationship known as the Monroe-Kelly doctrine. Small
increases in brain volume does not lead to immediate increase in ICP
because of the ability of the CSF to be displaced into the spinal canal,
as well as the slight ability to stretch the falx cerebri between the
hemispheres and the tentorium between the hemispheres and the
cerebellum. However, once the ICP has reached around 25 mmHg,
small increases in brain volume can lead to marked elevations in ICP.
Traumatic brain injury is a devastating problem with both high
mortality and high subsequent morbidity.
Injury to the brain occurs both at the time of the initial trauma (the
primary injury) and subsequently due to ongoing cerebral ischemia (the
secondary injury). Cerebral edema, hypotension, and axonal hypoxic
conditions are well recognized causes of this secondary injury.
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In the intensive care unit raised intracranial pressure (intracranial
hypertension) is seen frequently after a severe diffuse brain injury and
leads to cerebral ischemia by compromising cerebral perfusion.
The difference between the ICP and the mean arterial pressure within
the cerebral vessels is termed the cerebral perfusion pressure
(CPP)(cerebral perfusion pressure is calculated by subtracting the
intracranial pressure from the mean arterial pressure CPP=MAP-ICP),
the amount of blood able to reach the brain. One of the main dangers of
increased ICP is that it can cause ischemia by decreasing cerebral
perfusion pressure. Once the ICP approaches the level of the mean
systemic pressure, it becomes more and more difficult to squeeze blood
into the intracranial space. The body’s response to a decrease in CPP is
to raise blood pressure and dilate blood vessels in the brain. This results
in increased cerebral blood volume, which increases ICP, lowering CPP
further and causing a vicious cycle. This results in widespread
reduction in cerebral flow and perfusion, eventually leading to ischemia
and brain infarction. Increased blood pressure can also make
intracranial hemorrhages bleed faster, also increasing ICP.
Highly increased ICP, if caused by a one-sided space-occupying
process (eg. an haematoma) can result in midline shift, a dangerous
condition in which the brain moves toward one side as the result of
massive swelling in a cerebra hemisphere. Midline shift can compress
the ventricles and lead to buildup of CSF.[Prognosis is much worse in
patients with midline shift than in those without it. Another dire
consequence of increased ICP combined with a space-occupying
process is brain herniation (usually uncal or cerebellar), in which the
brain is squeezed past structures within the skull, severely compressing
it. If brainstem compression is involved, it may lead to decreased
respiratory drive and is potentially fatal. This herniation is often
referred to as "coning".
Major causes of morbidity due to increased intracranial pressure are due
to global brain infarction as well as decreased respiratory drive due to
brain herniation.
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H. Intracranial Hypertension
Minimal increases in ICP due to compensatory mechanisms are known
as stage 1 of intracranial hypertension.
When the lesion volume continues to increase beyond the point of
compensation, the ICP has not other resource, but to increase. Any
change in volume greater than 100-120 mL would mean a drastic
increase in ICP. This is stage 2 of intracranial hypertension.
Characteristics of stage 2 of intracranial hypertension include
compromise of neuronal oxygenation and systemic arteriolar
vasoconstriction to increace MAP and CPP.
Stage 3 of the intracranial hypertension is characterised by a sustained
increased ICP, with dramatic changes in ICP with small changes in
volume. In stage 3, as the ICP approaches the MAP, it becomes more
and more difficult to squeeze blood into the intracranial space. The
body’s response to a decrease in CPP is to raise blood pressure and
dilate blood vessels in the brain. This results in increased cerebral blood
volume, which increases ICP, lowering CPP further and causing a
vicious cycle. This results in widespread reduction in cerebral flow and
perfusion, eventually leading to ischemia and brain infarction.
Neurologic changes seen in increased ICP are mostly due to hypoxia
and hypercapnea and are as follows: decreased LOC, Cheyne-Stokes
respirations, hyperventilation, sluggish dilated pupils and widened pulse
pressure.
I. Causes of increased ICP
Causes of increased intracranial pressure can be classified by the
mechanism in which ICP is increased:
a) Mass effect such as brain tumor, infarction with edema,
contusions, subdural or epidural hematoma, or abscess all tend to
deform the adjacent brain.
b) Generalized brain swelling can occur in ischemic-anoxia states,
acute liver failure, hypertensive encephalopathy, pseudotumor
cerebri, hypercarbia, and Reye hepatocerebral syndrome. These
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conditions tend to decrease the cerebral perfusion pressure but
with minimal tissue shifts.
c) Increase in venous pressure can be due to venous sinus
thrombosis, heart failure, or obstruction of superior mediastinal
or jugular veins.
d) Obstruction to CSF flow and/or absorption can occur in
hydrocephalus (blockage in ventricles or subarachnoid space at
base of brain, e.g., by Arnold-Chiari malformation), extensive
meningeal
disease
(e.g.,
infectious,
carcinomatous,
granulomatous, or hemorrhagic), or obstruction in cerebral
convexities and superior sagittal sinus (decreased absorption).
e) Increased CSF production can occur in meningitis,
subarachnoid hemorrhage, or choroid plexus tumor.
J. Signs and symptoms of increased ICP
In general, symptoms and signs that suggest a rise in ICP including
headache, nausea, vomiting, ocular palsies, altered level of
consciousness, and papilla oedema. If papilla oedema is protracted, it
may lead to visual disturbances, optic atrophy, and eventually
blindness.
In addition to the above, if mass effect is present with resulting
displacement of brain tissue, additional signs may include pupillary
dilatation, abducens (CrN VI) palsies, and the Cushing's triad.
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Cushing's triad involves an increased systolic blood pressure, a
widened pulse pressure, bradycardia, and an abnormal respiratory
pattern.In children, a slow heart rate is especially suggestive of high
ICP.
Irregular respirations occur when injury to parts of the brain interfere
with the respiratory drive. Cheyne-Stokes respiration, in which
breathing is rapid for a period and then absent for a period, occurs
because of injury to the cerebral hemispheres or diencephalon.
Hyperventilation can occur when the brain stem or tegmentum is
damaged.
As a rule, patients with normal blood pressure retain normal alertness
with ICP of 25 to 40 mmHg (unless there's concurrent tissue shift).
Only when ICP exceeds 40 to 50 mmHg do CPP and cerebral perfusion
decrease to a level that result in loss of consciousness. Any further
elevations will lead to brain infarction and brain death.
In infants and small children, the effects of ICP differ due to the fact
that their cranial sutures have not closed. In infants, the fontanels, or
soft spots on the head where the skull bones have not yet fused, bulge
when ICP gets too high.
Gunshot wound left fronto-parietal region entrance wound
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Intracerebellar haemorrhage shown by CT scan
K. Treatment of increased ICP
In addition to management of the underlying causes, major
considerations in acute treatment of increased ICP relates to the
management of stroke and cerebral trauma.
One of the most important treatments for high ICP is to ensure
adequate airway, breathing, and oxygenation, since inadequate oxygen
levels or excess carbon dioxide cause cerebral blood vessels to dilate
and ICP to rise. Inadequate oxygen also forces brain cells to produce
energy using anaerobic metabolism, which produces lactic acid and
lowers pH, which dilates blood vessels.
On the other hand, blood vessels constrict when carbon dioxide levels
are below normal, so hyperventilating a patient with a ventilator or bag
valve mask can temporarily reduce ICP but limits blood flow to the
brain in a time when the brain may already be ischemic. Artificially
ventilating a patient at a fast rate used to be a standard part of head
trauma treatment because of its ability to rapidly lower ICP, but the
chance of developing ischemia was later recognized to be too much of
a risk. Furthermore, the brain adjusts to the new level of carbon
dioxide after 48 to 72 hours of hyperventilation, which could cause the
vessels to rapidly dilate if carbon dioxide levels were returned to
normal too quickly.
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Now hyperventilation is used when signs of brain herniation are
apparent because the damage herniation can cause is so severe that it
may be worthwhile to constrict blood vessels even if doing so reduces
blood flow.
Another way to lower ICP is to raise the head of the bed, allowing for
venous drainage. A side effect of this is that it could lower pressure of
blood to the head, resulting in inadequate blood supply to the brain.
Another simple method used to lower ICP (particularly in trauma
cases) is to loosen neck collars and clothing. This method is more
useful is the patient is sedated and thus movement is minimal.
Sandbags may be used to further limit neck movement.
In the hospital, blood pressure can be artificially raised in order to
increase CPP, increase perfusion, oxygenate tissues, remove wastes
and thereby lessen swelling. Since hypertension is the body's ways of
forcing blood into the brain, medical professionals do not normally
interfere with it when it is found in a head injured patient. When it is
necessary to decrease cerebral blood flow, MAP can be lowered using
common antihypertensive agents such as calcium channel blockers.
Struggling can increase metabolic demands and oxygen consumption,
as well as increasing blood pressure. Thus children may be paralyzed
with drugs if other methods for reducing ICP fail. Paralysis allows the
cerebral veins to drain more easily, but can mask signs of seizures, and
the drugs can have other harmful effects.
Pain is also treated to reduce agitation and metabolic needs of the
brain, but some pain medications may cause low blood pressure and
other side effects.
Intracranial pressure can be measured by means of a lumbar puncture
or continuously with intracranial transducers (only used in
neurosurgical intensive care). A catheter can be surgically inserted into
one of the brain's lateral ventricles and can be used to drain CSF
(cerebrospinal fluid) in order to decrease ICP's. This type of drain is
known as an EVD (extra-ventricular drain).In rare situations when
only small amounts of CSF are to be drained to reduce ICP's, drainage
of CSF via lumbar puncture can be used as a treatment.
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BLOOD-BRAIN BARRIER
The blood-brain barrier (BBB) is the specialized system of capillary
endothelial cells that protects the brain from harmful substances in the
blood stream, while supplying the brain with the required nutrients for
proper function. Unlike peripheral capillaries that allow relatively free
exchange of substance across / between cells, the BBB strictly limits
transport into the brain through both physical (tight junctions) and
metabolic (enzymes) barriers. Thus the BBB is often the rate-limiting
factor in determining permeation of therapeutic drugs into the brain.
Additionally, BBB breakdown is theorized to be a key component in
central nervous system (CNS) associated pathologies. BBB
investigation is an ever growing and dynamic field studied by
pharmacologists, neuroscientists, pathologists, physiologists, and
clinical practitioners.
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L. Management ICP
- Prevention vasospasm  calcium channel blocker Nimodipine
- Prevention seizure phenytoin
- Treatment seizure  diazepam, lorazepam, calcium, barbiturates …
- Intracranial mass lesions  surgical decompression
- CSF retention
-
acute CSF drainage via ventricular drain
chronic CSF drainage via ventriculo-peritoneal shunt
reducing CSF formation
frusemide (Lasix) by interfering chloride transport
acetazolamide (Diamox) by interfering carbonic
anhydrase system
- Cerebral oedema 
Oedema due to hypoxia
A: due to vasogenic breakdown in BBB (Blood brain barrier) or
cytotoxic where BBB intact
- fluid restriction (not always)
- osmolar diuretics (mannitol) reduction cerebral
B: oedema via intact BBB plus additional renal excretion
- loop diuretics (frusemide can prolong osmotic effect of
mannitol /ethacrynic acid)
- steroids (poor research support)
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- Cerebral blood volume
- Maintain MAP within limits cerebral autoregulation - beta
blockade post head injury
- Head up position 30 degree, neck alignment and minimal hip
flexion
- Sedation, neuromuscular blockade
- avoiding large increases in CVP/intrathoracic pressure
- Hyperventilation PaCO2 35 mmHg
- Cerebral vasoconstriction - thiopentone, barbiturate coma
M. Decompressive craniectomy
Craniotomeis are holes drilled in the skull to remove intracranial
hematomas or relieve pressure from parts of the brain. As raised ICP's
may be caused by the presence of a mass, removal of this via
craniotomy will decrease raised ICP's.
CASE:
Abstract
(Ref.:Sherif El-Watidy, Abdelazeem El-Dawlatly, Zain A. Jamjoom, Essam ElGamal: Use of Transcranial Cerebral Oximeter as Indicator for Bifrontal
Decompressive Craniectomy. Journal of Anaesthesiology. 2004. Volume 8
Number 2.)
Objectives: The timing of bifrontal decompressive craniectomy (BDC) in patients
with intractable intracranial hypertension (IH) is crucial, and the decision to do
surgery is based primarily on invasive neuromonitoring. In this report the authors
show the efficacy of a non-invasive, near infrared transcranial cerebral
oximeter (TCCO) in the management of a patient with post-traumatic IH.
Clinical Presentation: A 14-year-old male patient who had severe head injury
following road traffic accident (RTA). His Glasgow Come Score (GCS) was 6/15.
Brain computerized tomography (CT) scan showed multiple brain contusions and
diffuse brain edema. He developed a state of IH that did not respond to standard
medical treatment. We have used TCCO for neuromonitoring, its readings showed
marked difference between the two cerebral hemispheres and this correlated well
with the clinical and radiological findings.
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Intervention: Because of the decreasing trend of cerebral oxygen saturation and
pupillary changes (anisocoria) BDC was performed.
The timing of surgery was appropriate as no brain infarction occurred. Following
surgery, TCCO readings were normal and the patient recovery was dramatic and
relatively quick.
Conclusion: TCCO may be an efficient Neuromonitoring tool in determining the
time for surgical interference in patients with IH following RTA.
Infrared transcranial cerebral oximeter
The patient was admitted to the intensive care unit and received standard treatment
for such cases: sedation and muscle relaxation, normothermia, mild hyperventilation
to keep PCO2 between 30-35 mmHg, mannitol, and dopamine infusion was titrated to
keep the mean BP 90 mmHg.
TCCO neuromonitoring was used which showed difference in the initial readings from
both cerebral hemispheres: left 57% and right 72%. The patient responded to
mannitol and the pupils came down to 2mm and became equal. We decided to
continue the same medical treatment and postpone surgical decompression. TCCO
readings in the first 6 hours were more or less similar to the initial readings with more
saturation in the right hemisphere.
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About 8 hours after admission there was an attack of bradycardia associated with
reduced oxygen saturation from cerebral hemispheres, right 65% and left 50%.
Repeat CT of the brain scan showed more apparent brain contusions surrounded with
oedema, more swelling of the left hemisphere with more shift of midline structures,
and complete obliteration of the basal cisterns. (see Fig. 2)
Immediately following CT scan, both pupils blown up with the left bigger than right.
An extra bolus of mannitol was given and the patient was quickly taken to the theatre
to undergo BDC. The patient head was kept slightly elevated on a horseshoe headrest.
The bicoronal skin incision runs at a variable distance behind the coronal suture, the
skin was raised together with the pericranium, and the temporalis fascia in one flap.
The temporalis muscle was detached and retracted posteriorly and inferiorly on both
sides. Two burr holes were done over the midline, the first one above the nasion (high
enough to avoid opening the frontal air sinus), and the second one at variable distance
behind the coronal suture (depending on the amount of bony decompression). Multiple
burr holes were then made along the planned line of bone cuts. We use either
craniotome or Gigli saw to cut the bone. After elevating the bone flap we performed
wide bilateral subtemporal bony decompression. The dura was opened on both sides
of the superior sagittal sinus which was cut between ligatures together with the falx
cerebri to allow simultaneous external herniation of both hemispheres without the risk
of brain incarceration. Dural cuts extend laterally to the base of the middle cranial
fossa and posteriorly parallel to the sinus. We closed skin in two layers leaving a
subgaleal drain.
Due to reflection of skin flap it is technically difficult to continue monitoring cerebral
oxygen saturation during surgery. Immediately following decompressive craniectomy,
the pupils came down to 2 mm and became equal but not reactive to light. The
cerebral oxygen saturation showed dramatic improvement (right hemisphere 85% and
left one 76%). Mannitol and dopamine were continued for three more days and then
tapered off. Nasogastric tube feeding was started on the second day and PCO2 was
maintained around 35 mmHg. Neurologic recovery following BDC was quick and
dramatic.
Two weeks later the trachea was extubated. The patient was able to open his eyes
spontaneously and obeyed verbal commands at times. GCS was 9-10/15 and his pupils
were equal and reactive to light. He had transient right arm weakness and dysphasia
for three weeks. Follow-up CT brain scans (Fig 3, 4) showed the resolution of brain
contusions, brain enema, and absence of brain infarction (Fig 5).
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Fig. 1
Fig.2
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Fig.3
Fig.4
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Fig.5
A decompressive craniectomy is a drastic treatment for increased ICP is,
in which a part of the skull is removed and the dura mater is expanded
to allow the brain to swell without crushing it or causing herniation.
The section of bone removed, known as a bone flap, can be stored in the
patient's abdomen (or in the freezer) and resited back to complete the
skull once the acute cause of raised ICP's has resolved.
N. Complications and Traumatic Brain Injury (TBI)
1. Postconcussion Syndrome
Within days to weeks of a head injury approximately 40 percent of
TBI survivors develop troubling symptoms called postconcussion
syndrome (PCS). A person need not have suffered a concussion or
loss of consciousness to develop the syndrome and many people
with mild TBI suffer from PCS. Symptoms include headache,
dizziness, vertigo (a sensation of spinning around or of objects
spinning around the person), memory problems, trouble
concentrating, sleeping problems, restlessness, irritability, apathy,
depression, and anxiety. These symptoms may last for a few weeks
after the head injury.
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The syndrome is more common in individuals who had
psychological symptoms, such as depression or anxiety, before the
injury. Treatment for PCS may include medicines for pain and
psychological conditions, and counselling to develop coping skills.
2. Seizures
About 25 percent of patients with brain contusions or haematomas
and about 50 percent of patients with penetrating head injuries will
develop seizures within the first 24 hours of the injury. These
seizures generally stop within a week. Doctors typically only treat
these seizures if they continue beyond a week. Seizures occurring
more than one week after injury are referred to as post-traumatic
epilepsy and are treated with medications. The medications may
need to be taken by the survivor for months or years following the
injury.
3. Hydrocephalus
Our brains continually produce and drain a fluid called
cerebrospinal fluid (CSF). When the brain is injured the drainage of
CSF may be affected and CSF may build up. This condition is
called hydrocephalus. The build-up of fluid can lead to increased
pressure in the brain. Hydrocephalus may begin during the early
stages of TBI but not be apparent until much later.
However, it usually is diagnosed within the first year after the
injury. Symptoms can include a decreased level of consciousness,
changes in behaviour, lack of coordination or balance, and loss of
the ability to hold urine. Treatment may include draining CSF
through a small plastic tube called a shunt. The shunt typically runs
under the skin from the head to the abdomen, where the fluid drains
and is reabsorbed by the body.
4. Leakage of CSF
Skull fractures can tear the membranes that cover the brain, leading
to leakage of CSF. While the leaking fluid may be trapped between
the membranes that surround the brain, it may also leak out of the
nose or ears. Surgery may be necessary to repair the fracture and
stop the leakage.
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5. Infections
Tears that let CSF out of the brain cavity can also allow air and
bacteria into the cavity. An infection of the membrane around the
brain is called meningitis and is a dangerous complication of TBI.
Most infections develop within a few weeks of the initial trauma
and result from skull fractures or penetrating injuries. Standard
treatment includes antibiotics and sometimes surgery to remove the
infected tissue.
6. Damaged Blood Vessels in the Brain
Surgery is necessary to repair an injured blood vessel responsible
for a hemorrhagic stroke. Ischemic strokes can be treated with a
drug that dissolves clots (a “thrombolytic” drug) if the stroke is
diagnosed within a few hours of the beginning of symptoms and
there is no evidence of bleeding in the brain. The drug can be given
intravenously or through a tube (catheter) that is inserted into an
artery in the groin and then advanced to the brain and then into the
clogged artery, where the medication is administered through the
catheter. Administering the drug through a catheter at the site of the
clot has a higher chance of success than intravenous medication but
is usually only performed at stroke centres by a team of specialists
that can be rapidly assembled twenty-four hours a day.
7. Cranial Nerve Injuries
Cranial nerves are nerves running from the brain through openings
in the skull and to areas in the head such as the eyes, ears, and face.
Skull fractures, especially at the base of the skull, can injure cranial
nerves. The seventh cranial nerve, called the facial nerve, is the
most commonly injured cranial nerve in TBI. An injured facial
nerve can result in paralysis of facial muscles. When facial muscles
are paralyzed, facial expressions such as smiling will not be
symmetrical. Nerve injuries may heal spontaneously. If they do not,
surgery may, in certain circumstances, be able to restore nerve
function.
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8. Pain
Pain is a common symptom of TBI and can be a significant
complication for conscious patients in the period immediately
following a TBI. Headache is the most common type of pain, but
other kinds of pain can also occur.
9. Complications for Unconscious Patients
Serious complications for patients who are unconscious, in a coma,
or in a vegetative state include bed or pressure sores of the skin,
repeated bladder infections, pneumonia or other life-threatening
infections, and the failure of multiple organs, such as the kidneys,
lungs, and heart.
10. General Trauma
When a TBI occurs there is usually trauma to not only the brain but
other parts of the body as well. These injuries require immediate
and specialized care and can complicate treatment of and recovery
from the TBI.
O. Disabilities from a TBI.
Disabilities resulting from a TBI depend upon the severity of the injury,
the location of the injury, and the age and general health of the
individual.
1. Cognitive Disabilities
“Cognition” describes the processes of thinking, reasoning, problem
solving, information processing, and memory. Most patients with
severe TBI, if they recover consciousness, suffer some cognitive
disability. People with moderate to severe TBI have more problems
with cognitive deficits than survivors with mild TBI, but a history of
several mild TBIs (for example, a football player) may have a
cumulative effect. Recovery from cognitive deficits is greatest within
the first six months after the injury and is usually more gradual after
that. Most improvements can be expected within two years of the
injury.
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2. Memory
The most common cognitive impairment among severely head-injured
survivors is memory loss, characterized by some loss of older
memories and the partial inability to retain new memories. Some of
these patients may experience post-traumatic amnesia, which can
involve the complete loss of memories either before or after the injury.
3. Concentration and attention
Many survivors with even mild to moderate head injuries who
experience cognitive deficits become easily confused or distracted and
have problems with concentration and attention.
4. Executive functioning
Many individuals with a mild to moderate TBI also have problems
with higher level, so-called “executive” functions, such as planning,
organizing, abstract reasoning, problem solving, and making
judgments. This disability may make it difficult to return to the same
job or school setting the individual was in before the injury.
5. Language and communication
Language and communication are frequent problems for TBI
survivors. Some individuals have trouble recalling words and speaking
or writing in complete sentences (called non-fluent aphasia). They may
speak in broken phrases and pause frequently. They are usually aware
of what is happening and may become extremely frustrated. Other
survivors may speak in complete sentences and use correct grammar
but for the listener the speech is pure gibberish, full of invented or
meaningless words (called fluent aphasia). TBI survivors with this
problem are often unaware that they make little sense and become
angry with others for not understanding them. Other survivors can
think of the appropriate language but cannot easily speak the words
because they are unable to use the muscles needed to form the words
and produce the sounds (called dysarthria). Speech is slow, slurred,
and garbled.
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6. Impairment of the Senses
Many TBI survivors have problems with one of the five senses,
especially vision. They may not register what they are seeing or may
be slow to recognize objects. Some individuals develop tinnitus, a
ringing or roaring in the ears. Others may develop a persistent bitter
taste in the mouth or complain of a constant foul smell. Some TBI
survivors feel persistent skin tingling, itching, or pain. Although rare,
these conditions are hard to treat.
7. Impairment of Hand-Eye Coordination
TBI survivors often have difficulty with hand-eye coordination.
Because of this, they may be prone to bumping into or dropping
objects or may seem generally unsteady. They may have difficulty
driving a car, working complex machinery, or playing sports.
8. Emotional and Behavioural Problems
Most TBI survivors have some emotional or behavioural problems.
Family members often find that personality changes and behavioural
problems are the most difficult disabilities to deal with. Emotional
problems can include depression, apathy, anxiety, irritability, anger,
paranoia, confusion, frustration, agitation, difficulty sleeping, and
mood swings. Problem behaviours may include aggression and
violence, impulsiveness, loss of inhibitions, acting out, being
uncooperative, emotional outbursts, childish behaviour, impaired selfcontrol, impaired self awareness, inability to take responsibility or
accept criticism, being concerned only with oneself, inappropriate
sexual activity, and alcohol or drug abuse. Sometimes TBI survivors
stop maturing emotionally, socially, or psychologically after the
trauma, which is a particularly serious problem for children and young
adults. Many TBI survivors who show psychiatric or behavioural
problems can be helped with medication and psychotherapy.
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P. Other Long-Term problems associated with TBI?
1. Alzheimer's Disease (AD)
AD is a degenerative disease in which the individual suffers
progressive loss of memory and other cognitive abilities. Recent
research suggests an association between head injury in early
adulthood and the development of AD later in life; the more severe
the head injury, the greater the risk of developing AD. Some evidence
indicates that a head injury may interact with other factors to trigger
the disease and may hasten the onset of the disease in individuals
already at risk.
2. Parkinson's disease and other motor problems
Parkinson's disease may develop years after TBI if the part of the
brain called the basal ganglia was injured. Symptoms of Parkinson's
disease include tremors, rigidity or stiffness, slow movement or
inability to move, a shuffling walk, and stooped posture. Despite
many scientific advances in recent years, no cure has yet been
discovered and the disease progresses in severity. Other movement
disorders that may develop after TBI include tremor, uncoordinated
muscle movements, and sudden contractions of muscles.
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The consequences of brain damage are as follows:
Behavioral/ Personality
CognitiveIntellectual
Emotional
PerceptualPerceptual Motor
Social Disabilities
1. Lack of goal-directed behavior
1. Disorders of consciousness
1. Apathy
1. Reduced motor speed
1. Social withdrawal
2. Lack of initiation
2. Disorientation
2. Impulsivity
2. Reduced eye-hand
coordination
2. Lack of acceptance by family
associates
3. Poor self-image, reduced self
worth
3. Memory deficits
3. Irritability
3. Poor depth perception
3. Family role identity problems
4. Spatial disorientation
4. Marital stress
5. Poor figure-ground perception
5. Sexual dysfunction
6. Auditory perceptual deficits
6. Inappropriate social behaviors
7. Anosognosia
7. Loss of leisure skills and
interests
4. Denial of disability or its
consequences
5. Aggressive behavior
4. Decreased abstraction
4. Aggressiveness
5. Decreased learning abilities
5. Anxiety
6. Language-communication
deficits
6. Depression
6. Childlike behavior
7. Emotional liability
7. General intellectual deficits
7. Bizarre, psychotic ideation and
behavior
8. Silliness
8. Deficits in processingsequencing information
8. Loss of sensitivity and concern for
others: selfishness
9. Dependency, passivity
10. Indecision
11. Indifference
8. Autotopagnosia
8. Need for structure
9. Tactile, auditory, visual neglect
9. Illogical thoughts.
9. Legal infractions
10. Apraxias
10. Poor judgment
10. Dependence in legal-business
affairs
11. Poor quality control
12. Inability to make
decisions
12. Slovenliness
13. Poor initiative
11. Unemployment-financial
difficulties
12. Inability to profit from
experience
13. Sexual disturbances
14. Drug, alcohol abuse
14. Verbal motor
perseveration
15. Confabulation
16. Difficulty on
generalization
17. Short attention span
18. Distractibility
19. Fatigability
20. Perplexity
21. Dyscalculia
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Conclusions
Of all types of injury, those to the brain are among the most likely to result in
death or permanent disability. Brain injury is the leading cause of death and
disability worldwide. Traumatic brain injury is the leading cause of seizure
disorders.
Every year, approximately millions of people sustain a head injury. Most of
these injuries are minor because the skull provides the brain with considerable
protection. The symptoms of minor head injuries usually go away on their own.
More than half a million head injuries a year, however, are severe enough to
require hospitalization. Learning to recognize a serious head injury, and
implementing basic first aid, can make the difference in saving someone's life. In
patients who have suffered a severe head injury, there is often one or more other
organ systems injured.
A head injury is any trauma that leads to injury of the scalp, skull, or brain.
These injuries can range from a minor bump on the skull to a devastating brain
injury. Head injury can be classified as either closed or penetrating. In a closed
head injury, the head sustains a blunt force by striking against an object. In a
penetrating head injury, an object breaks through the skull and enters the brain.
(This object is usually moving at a high speed like a windshield or another part
of a motor vehicle.) A concussion is a type of closed head injury that involves
the brain.
About 25 percent of patients with brain contusions or haematomas and about 50
percent of patients with penetrating head injuries will develop seizures within
the first 24 hours of the injury. These seizures generally stop within a week.
Doctors typically only treat these seizures if they continue beyond a week.
Seizures occurring more than one week after injury are referred to as posttraumatic epilepsy and are treated with medications.
Cognitive symptoms arising out of the head injury/brain damage may include
communication problems, reduced ability to process information, memory loss,
impaired judgment, spatial disorientation, and concentration problems.
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The physical problems caused by head injury/brain damage can include pain,
seizures, speech impairment, visual impairment, problems with balance,
sleeplessness, fatigue, and loss of taste and smell.
The emotional problems resulting from head injury/brain damage may include
inability to initiate activities, anxiety, depression, mood swings and difficulty in
completing tasks without reminders, impulsive behaviour, and feelings of
agitation.
Traumatic brain injury can range from relatively mild to catastrophically severe
depending on multiple factors including degree of force, multiple trauma,
neurological complications, and timeliness of emergency medical treatment.
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