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.
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.
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
post-traumatic amnesia (PTA), and loss of
consciousness (LOC).
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
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.
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.
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):
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.
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.
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 34-38mmHg
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
15-30 degree.
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.
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.