Transcript Primary injury

Traumatic brain injury (TBI), causes
substantial disability and mortality.
It occurs when a sudden trauma
damages the brain and disrupts
normal brain function.
TBI may have profound physical,
psychological, cognitive, emotional,
and social effects.
Pathophysiology
TBI may be divided into primary injury
and secondary injury.
Primary injury is induced by mechanical
force and occurs at the moment of injury.
Secondary injury is not mechanically
induced. It may be delayed from the
moment of impact, and it may superimpose
injury on a brain already affected by a
mechanical injury.
Primary injury:
The 2 main mechanisms that cause
primary injury are:
Contact (as an object striking the
head or the brain striking the inside of
the skull)
Acceleration-deceleration.
Primary injury due to contact may
result in; injury to the scalp, fracture to
the skull and surface contusions.
Contusions are distinct areas of
swollen brain tissue,typically found on
the poles of the frontal lobes, the
inferior aspects of the frontal lobes, the
cortex above and below the operculum
of the sylvian fissures, and the lateral
and inferior aspects of the temporal
lobes.
Primary injury due to accelerationdeceleration results from unrestricted
movement of the head and leads to
shear, tensile, and compressive
strains.
These forces can cause intracranial
haematoma or diffuse axonal injury
(injury to cranial nerves and the
pituitary stalk.
Intracranial haematoma is the most common cause
of death and clinical deterioration after TBI.
Haematomas may be:
Epidural haematomas caused by fracture of the
temporal bone and rupture of the middle
meningeal artery, clotted blood collects between
the bone and the dura.It can grow quickly creating
pressure against the brain tissue.
Subdural haematomas are usually caused by
rupture of the bridging veins in the subdural space.
They can grow large enough to act as mass
lesions, and they are associated with high
morbidity and mortality rates.
Subarachnoid haematomas result from damage
to blood vessels in the posterior fossa stalk.
Diffuse axonal injury (DAI) is one of the most
common and important pathologic feature of TBI.
It constitutes mostly microscopic damage, and it is
often not visible on imaging studies.
The main mechanical force that causes DAI is
rotational acceleration of the brain, resulting in
unrestricted head movement.
Rotational acceleration produces shearing and
tensile forces, and axons can be pulled apart at
the microscopic level.
Microscopic evaluation of the brain tissue often
shows numerous swollen and disconnected
axons.
Rapid stretching of axons is thought to damage
the axonal cytoskeleton and, therefore, disrupt
normal neuron function.
Secondary injury:
It may occur hours or even days after
the inciting traumatic event.
Injury may result from impairment or
local declines in CBF after TBI as a
result of local edema, haemorrhage or
increased ICP.
As a result of inadequate perfusion,
cellular ion pumps may fail, causing a
cascade involving intracellular
calcium and sodium which may
contribute to cellular destruction.
Excessive release of excitatory amino
acids, such as glutamate and
aspartate, exacerbates failure of the
ion pumps.
As the cascade continues, cells die,
causing free radical formation,
proteolysis, and lipid peroxidation.
These factors can ultimately cause
neuronal death.
To summarize causes of secondary
brain injury:
Hypotension
Hypoxaemia
Hypercarbia
Hyperthermia
Hyperglycaemia
Hypoglycaemia
Hyponatraemia
Seizures
Infection
Severity
Head injuries can be classified into mild,
moderate, and severe.
The Glascow Coma Scale (GCS),is the
most commonly used system for classifying
TBI severity;
TBI with a GCS of 13 or above is mild, 9–
12 is moderate, and 8 or below is severe.
Other classification systems are also used
to help determine severity; duration of posttraumatic amnesia (PTA), and loss of
consciousness (LOC).
Severity of traumatic brain
injury
GCS
Mild
13-15
PTA
LOC
Less
than 1
day
0-30 min.
Moderate 9-12
1-7 days
30min.24hrs.
Severe
More
than 7
days
More
than
24hrs.
3-8
Signs and symptoms
Symptoms are dependent on the injury's severity:
•
With mild TBI, the patient may remain conscious
or may lose consciousness for a few seconds or
minutes.
• Other symptoms of mild TBI include; headache,
vomiting, nausea, lack of motor coordination,
dizziness, difficulty balancing, lightheadedness,
blurred vision or tired eyes, ringing in the ears, bad
taste in the mouth, fatigue or lethargy, and
changes in sleep patterns.
• Cognitive and emotional symptoms include;
behavioral or mood changes, confusion, and
trouble with memory, concentration, attention, or
thinking.
A person with a moderate or severe TBI
may have a headache that does not go
away, repeated vomiting or nausea,
convulsions, an inability to awaken,dilation
of one or both pupils,slurred speech,
aphasia , dysarthria, weakness or
numbness in the limbs, loss of
coordination, confusion, restlessness, or
agitation.
Common long-term symptoms of
moderate to severe TBI are changes in
appropriate social behaviour, deficits in
social judgment, and cognitive changes,
especially problems with sustained
attention, processing speed, and executive
functioning.
When the pressure within the skull,ICP rises too
high, it can be deadly.
Signs of increased ICP include decreasing level of
consciousness, paralysis or weakness on one side
of the body, and a blown pupil, one that fails to
constrict in response to light .
Cushing's triad, a slow heart rate with high blood
pressure and respiratory depression is a classic
manifestation of significantly raised ICP.
Anisocoria, unequal pupil size, is another sign of
serious TBI.
Abnormal posturing, a characteristic positioning of
the limbs caused by severe diffuse injury or high
ICP, is an ominous sign.
Small children with moderate to severe TBI may
have some of these symptoms.
Other signs seen in young children include
persistent crying, inability to be consoled,
listlessness, refusal to nurse or eat and irritability.
Diagnosis
Neurological examination and assigning a
GCS Score.
Neuroimaging helps in determining the
diagnosis and prognosis and proposed
treatment.
The preferred radiologic test in the
emergency setting is computed
tomography (CT): it is quick, accurate,
and widely available.
Followup CT scans may be performed
later to determine whether the injury has
progressed.
Magnetic resonance imaging (MRI) can
show more details than CTas detecting
injury characteristics such as diffuse axonal
injury. However, MRI is not used in the
emergency setting.
X-rays are still used for head injuries that
are so mild that they do not need imaging
or severe enough to merit the more
accurate CT.
Angiography may be used to detect
blood vessel pathology.
Electroencephalography and
transcranial doppler may also be used.
Complications
Posttraumatic seizures;
frequently occur after moderate or
severe TBI, they are usually general or
partial.
Immediate seizures occur in the first 24
hours.
Early seizures occur in the first 2-7 days.
Late seizures occur after 7 days.
Temkin showed that prophylactic use of
phenytoin is effective during the first week
after TBI.
He recommended discontinuation after 1
week if no seizures develop because of its
lack of effect in preventing late seizures.
Hydrocephalus is characterized as
communicating or noncommunicating;
Noncommunicating hydrocephalus
occurs secondary to an obstruction in
the ventricular system before the
point at which CSF exits the fourth
ventricle.
Communicating hydrocephalus is the
most common form after TBI and
occurs when the obstruction is in the
subarachnoid space.
Deep vein thrombosis
-DVT is common in persons with TBI, with
an incidence as high as 54%.
-Risk factors for DVT include; immobility,
lower extremity fracture, paralysis, and
disruption in coagulation and fibrinolysis.
-DVT may cause pulmonary embolism,
postthrombotic syndrome or recurrence.
-DVT best detected by venous Doppler
ultrasonography and contrast-enhanced
venography.
-Prophylaxis for DVT should be started as
soon as possible.
Heterotopic ossification is described
as ectopic bone formation in the soft
tissue surrounding the joints,in TBI, its
incidence is 11-76%.
-It causes joint pain and decreases
range of motion ,it is often associated
with low-grade fever, peri-articular
swelling, peri-articular warmth, and
peri-articular erythema.
-The risk of heterotopic ossification is
greatest during the first 3-4 months
after injury.
Spasticity is defined as velocitydependent increase in tone.
It is found in an estimated 25% of
patients with TBI.
-First-line treatment for spasticity is
correct positioning of the involved
body segment and exercises.
-Second-line treatment include
splinting, casting and other
modalities.
GIT and urinary tract complications
remain among the most common
sequelae in patients with TBI.
-Most frequent GIT complications are;
stress ulcers, dysphagia, bowel
incontinence, and elevated levels of
liver function tests.
-Urinary tract complications include;
urethral strictures, infections, and
urinary incontinence.
Posttraumatic agitation is common after
TBI. Furthermore, aggression was
consistently associated with depression.
Insomia is common in TBI patients. They
may have nighttime awakenings and longer
sleep-onset latency.
Posttraumatic headache in 38%.
Posttraumatic depression in 40% after
TBI, it is further associated with cognitive
decline, anxiety disorders, substance
abuse, dysregulation of emotional
expression, and aggressive outbursts.
Management
Monitoring:
This is essential in severe TBI.
It includes; ECG, invasive arterial
blood pressure, pulse oximetry,
central venous pressure, urinary
catheter, naso-gastric vs oro-gastric
tube (in case of base skull fracture),
frequent neurological examination,
temperature and capnography.
Maintenance of cerebral
perfusion pressure(CPP):
This is achieved by maintaining MAP
above 90mmHg and preventing
increases in ICP,to be between
20-25mmHg.
CPP = MAP – ICP
Maintaining MAP
Treating hypovolaemia by 0.9% NaCl/
colloids/P-RBCs/FFP as indicated.
Avoid glucose containing fluids unless
there is hypoglycaemia (blood sugar
should be between 4-7 mmols).
Start early enteral feeding as,TBI patients
have induced hypermetabolic
and hypercatabolic state resulting in
increased energy and protein.
Use inotropes (noradrenaline- dopamine),
if other causes of hypotension are treated.
Controlling ICP
Raised ICP leads to secondary brain
injury.
It is treated by; osmotherapy, analgesia,
sedation, optimal ventilation, surgical
and positioning of patient.
Osmotherapy
Mannitol induces changes in blood
rheology and increases cardiac output,
leading to improved CPP and cerebral
oxygenation.
Improvements in cerebral oxygenation
induce cerebral artery vasoconstriction and
subsequent reduction in cerebral blood
volume and ICP.
Mild dehydration after osmotherapy is
desirable and may improve cerebral
edema.
Also it decreases CSF production by up to
50%, lead to prolonged ICP decrease.
Mannitol has several limitations;
• Hyperosmolality is a common
problem, and a serum osmolarity
>320 mOsmol/L is associated with
adverse renal and central nervous
system effects.
• Accumulation of mannitol in cerebral
tissue may lead to a rebound
phenomenon and increased ICP.
The most promising solution investigated
as possible substitute for mannitol; is
hypertonic saline (HTS).
Serum Na is maintained between 145 and
155 mmol/L in all patients with TBI.
To start osmotherapy,250-mL bolus of 3%
HTS is administered through a central
venous cannula.
This dose is repeated until ICP is
controlled or a Na level of 155 mmol/L is
achieved.
The serum Na is maintained at this level
until ICP has stabilized and then gradually
allowed to normalize.
If ICP control is still problematic after
3–4 days of HTS therapy, boluses of
furosemide are administered in an
effort to mobilize tissue Na.
Serum sodium and potassium
concentrations are monitored four
hourly on a blood gas analyzer.
The permeability of the BBB to sodium is low.HTS
produces an osmotic gradient between the
intravascular and intracellular compartments,
leading to shrinkage of brain tissue (where BBB is
intact) and therefore reducing ICP.
The selectivity of the BBB to NaCl is more than
that of mannitol making it potentially a more
effective osmotic drug.
HTS augments volume resuscitation and
increases circulating BV, MAP, and CPP.
HTS restores the neuronal membrane potential,
maintains BBB integrity, and modulates the
inflammatory response by reducing adhesion of
leukocytes to endothelium.
Analgesia and Sedation
Morphine or fentanyl can be used for analgesia
but with caution for their respiratory depression in
case patient is spontaneously breathing.
Remifentanyl can be used in ventilated patients.
Propofol is sedative of choice especially in first 48
hours. It causes cerebral metabolic suppression
and has neuroprotective effect. Using propofol in
doses more than 5mg/Kg and for longer than
48hrs;
Midazolam should replace propofol for sedation.
(for fear of propofol infusion syndrome).
Mechanical ventilation
In TBI patients, hypoxia, hypercarbia /
hypocarbia should be prevented.
PaO2 should be above 100mmHg and
SpO2 above 95%.
Mechanical ventilation should be started at
GCS 8.
PaCO2 in first 24hrs should be 3438mmHg and mild hyperventilation can be
started for PaCO2 to be 32-35mmHg in
case of increased ICP.
Monitor end tidal CO2 and perform blood
gases 15-20 min. after any change in
ventilatory parameters.
Neuromuscular blockade
May be considersd to facilitate
endotracheal intubation.
In cases of difficult ventilation inspite
of adequate sedation/analgesia.
Use of neuromuscular blockade may
mask seizure activity, increase risk of
pneumonia and cause critical illness
neuropathy.
Patient positioning
Patient head should be in neutral
position with head of bed elevated 1530 degree.
Neck collar should be applied
whenever there is doubt of cervical
spine injury.
Surgical Intervention
Whenever decided by neurosurgeon
to decrease intracranial hypertension.
Surgery can be performed on mass
lesions or to eleminate objects that
penetrated the brain.
Mass lesions are like contusions or
haematomas causing significant shift
of intracranial structures.
Maintenance of haematological
parameters
Monitor HCT or haemoglobin level as
CBF is influenced by blood viscosity
which increases by increase in HCT.
CBF is reduced by HCT levels above
50% and increased by HCT levels
below 30%.
HTC of 30-34% is suggested to be
best for optimal oxygen delivery to
brain tissue.
Control of seizures
Seizure activity in TBI patients may
cause secondary brain damage as a
result of increased metabolic
demands, raised ICP and excess
neurotransmitter release.
Benzodiazepines should be started
together with phenytoin .
Adequate sedation with propofol
reduces seizure activity and raises
seizure threshold.
Treating hyperpyrexia
Increase in body temperature should
be treated agressively; paracetamol,
cooling blanket, cool sponging and ice
packs.
Hyperthermia increases metabolic
demand and aggrevates the
condition.
Monitoring renal function
Urine output should be 0.51ml/Kg/min.
Diabetes insipidus should be
suspected if urine output is more than
250ml/hr, for more than 3hrs. and
specific gravity less than
1005,confirmed by serum and urine
osmolalities.
If confirmed , start desmopressin.
Monitoring increase in ICP
CT scan should be done on
admission and repeated whenever
there is change in symptoms or signs.
Frequent neurological examination is
essential.
Hourly recording of GCS, hourly
recording of pupil size and reaction.
Monitoring ICP if available.
Figure 1. Suggested algorithm for cerebral resuscitation after traumatic brain injury, adapted from
the Brain Trauma Foundation and the European Brain Injury Consortium Guidelines and modified to
replace mannitol with hypertonic saline for osmotherapy.
White H et al. Anesth Analg 2006;102:1836-1846