2. ● Traumatic brain injury (TBI) is one of the top causes of morbidity
and mortality in paediatrics.
● The modern management of severe TBI in children on intensive
care unit focuses on preventing secondary brain injury to improve
outcome.
● Previously published studies conducted in other countries such as
in the United States, Australia and New Zealand have estimated
the rate of childhood brain injury to range from 75 to 1,373 per
100,000 among children aged below 15 years old
● Head Injury was the fifth (7.86%) commonest cause of
hospitalisation in MOH hospital Malaysia in 2014.
3. ● Cerebral Perfusion (CPP) = mean arterial pressure (MAP) – ICP considered the driving pressure for
cerebral blood flow and perfusion.
● In the normal brain, cerebral autoregulation maintains CPP within a specific range to couple oxygen
delivery with cerebral metabolic rate.
● TBI impairs the cerebral autoregulatory capacity making brain vulnerable to both systemic hypotension
and raised ICP.
● Defining an ideal CPP for children is challenging and the current guidelines support maintaining a
minimum CPP of 40 mmHg and a threshold of 40-50 mmHg.
● Very high CPP with use of vasopressors and fluids is associated with serious systemic toxicity and does
not give better outcomes. Very high CPP can increase cerebral blood volume leading to an increasing
ICP and also increase vasogenic oedema by increasing the hydrostatic pressure across the capillary
bed.
4. ● Hypotension or shock any time after injury can have major implications for clinical
outcome and should be actively prevented and aggressively treated with fluid boluses and
vasoactive agents.
● While hypotension can potentially cause brain ischemia, hypertension can exacerbate
vasogenic oedema in the cerebral parenchyma
● As the primary injury often impairs cerebral autoregulation, the cerebral perfusion may
become directly dependent on the mean arterial pressure.
Circulatory support
5. ● Early airway control is recommended to avoid hypoxemia, hypercarbia and aspiration.
● The adequacy of oxygenation and ventilation should be measured continuously with pulse
oximetry and end-tidal carbon dioxide (CO2) monitoring respectively and serial blood gas
measurements.
● Arterial PaO2 should be maintained above 11 kPa (saturations > 90%) and
PaCO2 between 4.5-5 kPa.
● Hypercapnea causes vasodilatation leading to cerebral hyperaemia and hypocapnea
causes ischemia by cerebral vasoconstriction.
6. ● Sedation, analgesia and neuromuscular blockade
● Any noxious stimulus increases ICP and cerebral metabolic demand for oxygen
● Sedation and analgesia can :
Reduces anxiety and pain
Facilitates ventilation and general intensive care management helps reduce the cerebral oxygen demand reduce secondary brain injury.
● Combination of benzodiazepines and opioids is most often used.
This combination can cause hypotension, careful titration and monitoring of blood pressure to minimize risks of cerebral ischemia.
● Neuromuscular paralysis :
Help to reduce airway and intrathoracic pressure which improves the cerebral venous return.
Can prevent shivering and posturing (the lack of skeletal muscle movement) helps to reduce cerebral metabolic demand.
● Main disadvantage of neuromuscular blockade
Masking of clinical seizures (ideally seizure to be monitored by continuous EEG)
Its continuous use can also induce myopathy, increase length of ventilation, and cause nosocomial pneumonia and cardiovascular side effects.
7.
8. •Mild TBI (mTBI) — loss of consciousness for less than 30 minutes, an initial
Glasgow Coma Scale (GCS) or Pediatric GCS of 13–15 after 30 minutes of
injury onset, and PTA for not greater than 24 hours
•Uncomplicated — mTBI where there are no overt neuroimaging findings.
• Complicated — mTBI where there are intracranial abnormalities
(e.g., bruising or a collection of blood in the brain) seen on CT scan
or MRI.
•Moderate TBI — loss of consciousness and/or PTA for 1–24 hours and a
GCS of 9–12
•Severe TBI — loss of consciousness for more than 24 hours and PTA for
more than 7 days with a GCS of 3–8
(CDC, 2015).
21. maintain adequate oxygen delivery to the brain via a few principals:
o maintaining cerebral perfusion
o avoiding ischaemia
o decreasing the brain’s metabolic demand
22.
23. Maintaining Cerebral Perfusion
Cerebral perfusion pressure
Cerebral Perfusion Pressure (CPP) = Mean Arterial
Pressure (MAP) – Intracranial Pressure (ICP)
• An appropriate target CPP is around 40-60 mmHg
• aiming slightly lower for younger children (40-50mmHg for 0-5
year olds)
• slightly higher for older children (50-60mmHg for 6-17 year
olds).
24. Target MAP = the upper end of normal for age
• Reaching your target MAP is achieved either with fluid, if the
patient is fluid deficient, or inotropes.
• Measuring central venous pressure (CVP) can be helpful as an
indicator of the patient’s volume status. If it is low, you can
give a fluid bolus to improve blood pressure and CPP.
• If it is normal or high and the patient is hypotensive,
vasopressors will be more helpful.
• It is imperative to avoid hypotension, which reduces cerebral
perfusion pressure and can cause brain ischaemia; but it is also
important to avoid hypertension, which can worsen cerebral
oedema.
25. Target ICP = less than 20 mmHg
• If we rearrange the equation CPP = MAP – ICP, we can show that MAP = CPP +
ICP. Therefore, you can determine your target MAP by choosing an age
appropriate CPP and use 20 as your value for ICP.
• Normal ICP is usually considered to be 5–15 mmHg in a healthy
supine adult, 3–7 mmHg in children, and 1.5–6 mmHg in infants.
• ICP >20 mmHg is considered to be elevated, and this is
considered an important cause of secondary injury leading to
irreversible brain injury
26. Intracranial Pressure
• The Monroe Kellie Doctrine describes that the cranium is a closed system that
comprises of three components; brain mass (80%), blood (10%) and CSF (10%).
• If one of these components increases in size the others must decrease to maintain the
ICP. For example, if a patient sustains a traumatic brain injury, the resulting cerebral
oedema (which occurs maximally at 24-72 hours post-injury) causes an increase in
brain mass.
• As a result, the CSF will be displaced into the spinal canal to allow for the increased
brain mass. If that is not sufficient, then the volume of venous blood in the cranium will
decrease secondary to the increased intracranial pressure.
27. As the ‘Mass’ (e.g. haemorrhage, space occupying lesion, etc)
volume increases, to compensate and maintain ICP first CSF and
then blood is displaced. Eventually these mechanisms are
exhausted, and brain matter is then at risk of herniation.
28. • However, these compensatory measures have their limits and eventually
the rising pressure will force brain mass out of the cranium, known as
herniation.
• Clinically, uncal herniation presents as a unilateral fixed and dilated
pupil and is often fatal.
• Prior to this point, the patient will exhibit signs and symptoms of raised
ICP including pupillary dilatation, hypertension, bradycardia and
irregular respiratory effort (Cushing’s triad) and abnormal posturing,
although these are still late findings of elevated ICP and are therefore
very worrisome themselves.
29. Measuring ICP
• Many different devices can measure ICP, but the gold
standard is an external ventricular drain (EVD).
• This device places a probe inside the ventricle that
measures the ICP and can also be opened to drain
additional CSF to reduce ICP.
• Bolts are another commonly used device placed intra-
parenchymally which measures ICP continuously. Bolts
cannot be used to drain CSF or augment ICP as it is
solely a measuring device. Remember – the goal is to
keep ICP less than 20mmHg, or lower if symptomatic!
30. Reducing ICP
• head of the bed should be placed at 30° with the
patient’s head in the midline position to promote
cerebral venous drainage.
• If venous drainage is impaired, it will increase the
volume of blood in the cranium thereby increasing
the ICP. If an EVD is in place, CSF can be drained to
reduce ICP.
In order to reduce brain mass, 3%
NaCl can be used to raise the sodium
to 140-150.
• This raises the blood osmolarity and draws water out of the neurons which reduces cerebral oedema
and brain mass.
• Mannitol, an osmotic diuretic, can also be given to reduce blood viscosity by a similar mechanism and
therefore reduce ICP. However, the subsequent diuretic effect of mannitol can cause a drop in blood
pressure and therefore compromise your CPP
31. Finally, in cases of refractory
elevated ICP, a decompressive
craniotomy can turn a ‘closed
system’ into an ‘open system’,
reducing the risk of
herniation.
32. Avoiding
ischaemia
• Hypoxia causes cerebral vasodilation – since the
brain is receiving less oxygen per unit blood, it tries
to compensate by increasing the amount of blood it
receives.
• This increased blood flow can worsen cerebral
oedema and intra-cranial pressure. Hypoxia can
obviously cause ischemia in and of itself as well and
therefore should be avoided by giving supplemental
oxygen.
• In addition, anaemia should be avoided to help
maintain the oxygen carrying capacity of the blood
and oxygen delivery to the brain.
33. Maintain PaCO2 4.5 to 5.3 kPA
.
Decreasing the brain’s metabolic demand
Sedation, neuromuscular blockade and seizure prophylaxis
Glycaemic control
prevent persistent hyperglycaemia (Glucose > 10 mmol/L)
Temperature control
avoid hyperthermia as it significantly increases cerebral metabolic demands
34. Other Considerations
o Any coagulopathy that is present should be corrected to prevent any further risk of
intracranial bleeding.
o Good nursing care should include eye care, stress ulcer prophylaxis and compression
stockings for DVT prevention.
o Nutrition is required for tissue repair and adult data supports early nutritional support,
either enteral or parenteral.
35. Consider your target CPP and
manipulate your MAP and ICP
to achieve it.
Nurse head up at 30° and with the head in mid-
line to improve venous drainage of blood and
reduce ICP
3% saline and mannitol can be used to
increase the osmolality of the blood and draw
fluid out of the intracellular space, reducing
oedema and therefore ICP
ICP can be measured, and in some cases
altered, using devices such as bolts and drains
Reducing the metabolic demand
on the brain can be achieved
through maintaining normal
temperature and blood sugar,
and by medicating to sedate,
paralyse and prevent seizures.
TAKE HOME MESSAGE
Aiming for normal CO2 levels
and avoiding hypoxia through
mechanical ventilation optimise
cerebral blood flow
41. • The gold standard for monitoring ICP is an intraventricular catheter connected to an external pressure
transducer; the catheter is placed into one of the ventricles through a burr hole.[49,64,76] The catheter can also
be used for therapeutic CSF drainage and for administration of drugs.
• ICP monitoring, it is associated with a number of complications. These include risk of infection, hemorrhage,
obstruction, difficulty in placement, malposition, etc
Anterior fontanelle pressure monitoring
The anterior fontanelle of the human infant is open, making it an available site to measure ICP in an infant. Many
studies were conducted in the 1970s and 1980s to investigate the correlation
• On the same lines, Salmon et al.[73] studied the use of an applanation transducer (called the fontogram).
Laboratory and clinical studies were carried out, and it was found that the pressures recorded by the fontogram
corresponded to direct measurements of ICP through an invasive catheter; the correlation coefficient was 0.98
and P value <0.001, indicating a very good correlation. It was concluded that it was accurate to use fontanelle
pressure and ICP interchangeably.
Editor's Notes
So basically, make sure blood is getting to the brain and delivering oxygen to the tissues, whilst also decreasing the amount of oxygen the brain actually needs. Let’s think about each of those in more detail (although there is clearly overlap for many of the interventions we will discuss).
Your cerebral perfusion pressure (CPP) is the difference between your mean arterial pressure (MAP) and your intracranial pressure (ICP). In other words, it is the pressure gradient which drives cerebral blood flow. It is important to calculate and monitor CPP in TBI because the normal homeostatic mechanisms which maintain an adequate blood flow to the brain can be lost.
In order to maintain adequate oxygen delivery to the brain we can reduce its metabolic demand, thereby reducing its oxygen requirements. First off, medications to sedate and paralyse the patient reduce both the metabolic demand and the ICP. Paralysis using neuromuscular blockers reduces cerebral metabolic demand by preventing shivering, posturing and convulsions and improves cerebral venous drainage by reducing intrathoracic pressure. Seizure prophylaxis is started early as TBI patients are at risk for seizures and seizures both increase metabolic demand and ICP. It is important to remember to place a video EEG on these patients given their risk of seizures, especially if they are paralysed, as paralysis masks the convulsions that normally make seizures more easily detectable.
Carbon dioxide is a cerebral vasodilator. Hypercarbia (CO2 > 6 kPA) causes cerebral blood vessels to dilate, which worsens cerebral oedema and can raise ICP as per the Monro-Kellie Doctrine. Hypocarbia (CO2< 4 kPA) causes cerebral blood vessels to constrict and that can lead to ischaemia. Obviously, neither one of these are good ideas and should be avoided. To do this, these patients usually require intubation so that we can take over and control their ventilation to maintain a normal CO2 level
