The information found on this site is the personal opinion of the authors, and is intended to educate and interest, rather than to direct clinical management for specific patients. Copyright is shared between the author/s and this site. You may reproduce this content as long as the original source is credited. No information on this site may be reproduced for profit.

Protecting #1 – Neuroprotective strategies for Severe Traumatic Brain Injury

Manette Ness-Cochinwala, Buvana Dwarakanathan

Traumatic brain injury (TBI) is one of the top causes of morbidity and mortality in paediatrics. In the UK, head injury is the most common cause of death and disability in people aged between 1-40 years old. There are 1.4 million A&E visits in England for head injury each year and between one third and one half of these are for patients under 15 years old. That’s huge! Unlike other types of injuries, like a broken arm, where the majority of the damage occurs at the time of injury, further brain damage can occur after the time of injury through oedema, ischaemia and inflammation. This is where neuroprotective strategies come into play for severe TBI.

What neuroprotection looks like

A sedated, intubated patient with normal values for almost everything – except sodium!

In general, we have to maintain adequate oxygen delivery to the brain. This is accomplished via a few principals:

  • maintaining cerebral perfusion
  • avoiding ischaemia and
  • decreasing the brain’s metabolic demand

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).

Maintaining Cerebral Perfusion

Cerebral perfusion pressure

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.

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) and slightly higher for older children (50-60mmHg for 6-17 year olds). Considering the above equation, you can maintain CPP by either increasing the MAP or reducing the ICP. So what are appropriate target values?

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.

If your patient has refractory hypotension, consider ACTH deficiency. In 25% of paediatric patients with TBI, pituitary dysfunction has been reported in the acute phase

Target ICP = less than 20 mmHg

‘Normal’ ICP is 5-15 mmHg, but raised ICP is thought of as >20 mmHg. Evidence has shown reduced mortality benefit through maintaining the ICP below 20 mmHg after TBI. The clinical relevance of this comes when considering whether your blood pressure is adequate to maintain you CPP in a patient with TBI, before they have ICP monitoring. 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.

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.

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.

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.

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!

Reducing ICP

There are several mechanisms to reduce ICP based on the principals of the Monroe-Kellie Doctrine and these form a crucial part of neuroprotective strategy. First off, the 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 – something to be wary of!

Finally, in cases of refractory elevated ICP, a decompressive craniotomy can turn a ‘closed system’ into an ‘open system’, reducing the risk of herniation.

Avoiding ischaemia

Avoid Hypoxia

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.

Maintain PaCO2 4.5 to 5.3 kPA

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.

Decreasing the brain’s metabolic demand

Sedation, neuromuscular blockade and seizure prophylaxis

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.

Glycaemic control

Generally, it is advised to prevent persistent hyperglycaemia (Glucose > 10 mmol/L).  It should only be treated if it is truly persistent, as hypoglycaemia is much more dangerous and detrimental to an injured brain. First line treatment should be with reducing the dextrose concentration in IVF, and then only if it is truly persistent should an insulin drip be started. Target glucose concentration should not be ‘normal’, but only  <10 mmol/l, as tight glucose control has been shown to be detrimental given the incidence of accidentally induced hypoglycaemia.

Temperature control

As for temperature management, normothermia (36.5°C -37.5°C) is maintained either by use of anti-pyretics or cooling blankets. It is very important to avoid hyperthermia as it significantly increases cerebral metabolic demands. There has been much debate on the benefits of hypothermia but current evidence shows that early therapeutic hypothermia has no mortality benefit.

Other Considerations

  • Any coagulopathy that is present should be corrected to prevent any further risk of intracranial bleeding.
  • Good nursing care should include eye care, stress ulcer prophylaxis and compression stockings for DVT prevention.
  • Nutrition is required for tissue repair and adult data supports early nutritional support, either enteral or parenteral.

So to summarise…

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.

Aiming for normal CO2 levels and avoiding hypoxia through mechanical ventilation optimise cerebral blood flow

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.

Conclusion

Traumatic brain injury is a common cause of mortality and morbidity in paediatrics. These patients have already sustained significant damage at the time of initial injury and it is very important to manage them correctly in order to avoid any further damage and worsening neurological impairment.

Further reading (if so inclined)

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632392/
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146616/
  3. The Cool Kids trial – looking at therapeutic hypothermia in TBI:
    https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(13)70077-2/fulltext
  4. NICE guidance on head injury and early management:
    https://www.nice.org.uk/guidance/cg176/chapter/Introduction
  5. A review of non-invasive ICP monitoring: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5402331/
  6. 2019 guideline on paediatric TBI published in Pediatric Critical Care Medicine:
    https://journals.lww.com/pccmjournal/Fulltext/2019/03000/Management_of_Pediatric_Severe_Traumatic_Brain.8.aspx
  7. Nice review article of all things paediatric TBI: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4733454/pdf/WJCCM-5-36.pdf

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The information found on this site is the personal opinion of the authors, and is intended to educate and interest, rather than to direct clinical management for specific patients. Copyright is shared between the author/s and this site. You may reproduce this content as long as the original source is credited. No information on this site may be reproduced for profit. 2018, paediatricfoam.com