Immediate Management of Paediatric Traumatic Brain Injury

Traumatic brain injury (TBI) has been noted as a leading cause of death and disability in infants, children, and adolescence (Araki, Yokota and Morita, 2017). In the UK alone, it’s approximated 1.4 million individuals attend the emergency department (ED) with head injury, and of those, 33%-50% are children under the age of 15; on top of this, a fifth of those patients admitted have features suggesting skull fracture or brain damage – that’s no small figure (NICE, 2014)! The particular importance of TBI in the paediatric population is that the treatment and management approach differs to adults; this is largely due to the anatomical and physiological differences in children. Furthermore, neurological evaluation in children proves more complex. All in all, children are complicated, and it is of great importance that we are aware of these differences when a paediatric patient arrives at the ED with TBI presentations.

Why is the paediatric population at risk for TBIs?

To delve slightly deeper into physiology and anatomy, there are several reasons children are at high risk of acquiring serious injury from TBIs. The paediatric brain has higher plasticity and deformity. As such, their less rigid skulls and open sutures allow for greater shock absorbance and response to mechanical stresses (Ghajar and Hariri, 1992). This ‘shaking’ of the brain inside the skull can stretch and tear at blood vessels in the brain parenchyma, resulting in cerebral haemorrhage.

Children also have a larger head-to-body size ratio, making the probability of head involvement in injury consequently higher (in comparison to adults); the head is also relatively heavier in a child, making it more vulnerable (especially in injury caused by sudden acceleration).

Young children have weaker neck muscles on top of having relatively heavier heads. Ligaments in the neck are relied on for craniocervical stability more so than the vertebrae. Hence, not only are TBIs more likely, but craniocervical junction lesions can also result from traumatic injury.

How does TBI in children come about?

The common causes of TBI in the paediatric population varies with age (Araki, Yokota and Morita, 2017). Some of these causes can be seen in the table below, which has been adopted from Araki, Yokota, and Morita (2017).

Table 1 Injury characteristics according to age and development

How can TBI in children present?

  • History: dangerous mechanism of injury (e.g. road traffic accidents or fall from a height greater than 1 meter)
  • Glasgow Coma Scale (GCS) less than 15 (at 2 hours after injury)
  • Visible bleeding, bruise, swelling, laceration
  • Signs of base-of-skull fracture:
    •  ‘Panda’ eyes – haemotympanum
    • Battle’s sign – cerebrospinal fluid leakage from ear or nose
  • Seizure (ask about history of epilepsy)
  • Focal neurological deficit
  • Vomiting
  • Loss of consciousness
  • Amnesia lasting more than 5 minutes
  • Abnormal drowsiness 

Note some children won’t have any of these signs, but if there is any suspicion of possible TBI, it should be investigated further.

Immediate management

There are various causes to paediatric TBI – also subdivided into primary and secondary TBI. Primary TBI includes skull fractures and intracranial injury. Secondary TBI can be caused by diffuse cerebral swelling. Primary and secondary TBI will be managed similarly in initial treatment (i.e. in the ED). The goal of baseline treatment is to:

  1. maintain blood flow to the brain
  2. prevent ischaemia (and possible secondary injury)
  3. maintain homeostasis 

Analgesia, Sedation, Seizure Prophylaxis

A level of anaesthesia needs to be achieved to allow for invasive procedures, such as airway management and intracranial pressure (ICP) control. Normally opioids and benzodiazepines are using in combination for analgesia and sedation in children. Instances where a child presents with a severe TBI (defined as a ‘brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8’), a neuromuscular block is used to improve mechanical ventilation, stop shivering, and reduce metabolic demand.

Anticonvulsants have been used in children, in particular infants, as they have a lower seizure threshold. Risk factors for early onset of seizures in infants under the age of 2 include hypotension, child abuse, and a GCS of ≤ 8; note, all of which may occur as a result of, or preceding, a TBI! For severe paediatric TBI cases, immediate prophylactic administration of anticonvulsants has been recommended.

Maintaining Cerebral Perfusion

The gold standard to measure ICP is an external ventricular drain (EVD); which can be used not only to measure ICP but can also be opened to drain additional CSF to reduce ICP. An intraparenchymal intracranial pressure sensor is an immediate invasive method used to detect early increased ICP in children with TBI. Monitoring of both ICP and cerebral perfusion pressure (CPP) is considered standard practice in TBI management in both paediatric and adult populations, as it is associated with better outcomes.

CPP is the pressure gradient which allows for cerebral blood flow. If this pressure is not maintained, the brain will lose adequate blood flow (Ness-Cochinwala and Dwarakanathan, 2019). Elevated CPP can accelerate oedema and increase chances of secondary intracranial hypertension.

Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)

A CPP of around 40-60 mmHg (40-50mmHg in 0-5 year-olds and 50-60mmHg in 6-17 year-olds) is considered ideal. Achieving an adequate CPP can be done by increasing MAP or reducing ICP (using the above equation). Hence it is necessary to have a good understanding of what good target values for MAP and ICP are.

A good target value for MAP is the upper end of ‘normal’ for the child’s age. Reaching this can be done by using fluids (if fluid deficient) or by use of inotropes. The recommended ICP target is < 20mmHg (normal is between 5-15 mmHg and raised ICP is regarded as values over 20mmHg).

When thinking about ICP, it’s useful to remember a mass in the brain; a mass being possible haemorrhage or any other space-occupying lesion. In TBI, oedema is most prominent at around 24-72 hours post-injury. As a result of increased mass, the initial consequence is a displacement of cerebrospinal fluid (CSF) into the spinal cord. Following this, venous blood in the cranium will also be displaced.

If ICP is further elevated, herniation can result – which is serious and often fatal! Signs of uncal herniation can present as unilateral fixed and dilated pupil. Signs of raised ICP can include pupillary dilatation and series of responses known as the ‘Cushing’s Triad’: irregular, decreased respiration (due to impaired brainstem function), bradycardia, and systolic hypertension (widened pulse pressure). Cushing’s triad results from the response of the body to overcome increased ICP by increasing arterial pressure.

Using the Monroe-Kellie Doctrine as a guide, we can predict how to reduce ICP. One management is head positioning. Head-of-bed should be elevated to 30˚, with the head in mid-line position, to encourage cerebral venous drainage. The EVD can also be used to drain CSF.

Commonly, intravenous mannitol and hypertonic saline are used to manage intracranial hypertension in TBI. Mannitol is traditionally used at a dosage of 20% at 0.25-1.0 g/kg – this is repeatedly administered. The plasma osmolality of the patient needs to be kept a close eye on; it should be ≤ 310 mOsm/L. 3% NaCl can be used to raise sodium levels to 140-150 mEg/L – this is slightly higher than normal sodium levels as a higher blood osmolarity will pull water out of neurons and brain cells osmotically and reduce cerebral oedema (Kochanek et al., 2019). Mannitol works in the same manner, however, use with caution as mannitol, being an osmotic diuretic, can cause blood pressure drops and compromise CPP! In last-resort emergency cases, where ICP need to be immediately reduced, a decompressive craniotomy can be performed.

Intravascular Volume Status

Measuring the patient’s central venous pressure (CVP) is a good indicator of the child’s volume status; 4-10 mmHg have been used as target thresholds. Alternatively, you can also monitor urine output (>1mL/kg/hr), blood urea nitrogen, and serum creatinine. Low volume status should be corrected with a fluid bolus. If the patient’s volume status is normal or high, but they remain hypotensive, vasopressors may improve blood pressure. At all costs, hypotension must be avoided, as if can lead to reduced cerebral perfusion and lead to brain ischaemia; on the other end, hypertension can cause severe cerebral oedema and should also be kept an eye on.

Other considerations​ - There have been reports of pituitary dysfunction in 25% of paediatric TBIs (during the acute phase). Do consider this if the patient had refractory hypotension – keep ACTH deficiency in mind!

Ischaemia

Prevent hypoxia at all costs! Hypoxia goes hand-in-hand with cerebral vasodilation – and as we already know, this increases the pressure in the cranium. Additionally, with hypoxia, there will be ischaemia. A minimum haemoglobin target of 7.0 g/dl is advised in a severe paediatric TBI case.

Other considerations​ - Whilst we are on the blood topic, also take care to correct and control any coagulopathies.

Ventilation

At a Paediatric Glasgow Coma Scale (PGCS) of less than 8, airways must be secured with a tracheal tube and mechanical ventilation commenced. SpO2 should be maintained at greater than 92%.

Of course, hypercapnia (CO2 > 6 kPa) and hypocapnia (CO2 < 4 kPa) are both not ideal, and we should maintain paCO2 at 4.5 – 5.3 kPa. However, some sources have suggested a quick fix to reduce ICP is to acutely hyperventilate the patient (as low CO2 results in cerebral vasoconstriction) – it’s suggested that paCO2 can safely go as low as 2.67 kPa before ischaemia kicks in! Mild hyperventilation is recommended (3.9 – 4.6 kPa)(Araki, Yokota and Morita, 2017).

Decreasing Metabolic Demand of the Brain

Body Temperature

What we want is to prevent hyperthermia, as it increases cerebral metabolic demands. Normothermia (36.5˚C – 37.5˚C) can be maintained by use of cooling blankets or antipyretics. There has been debate on whether therapeutic hypothermia has shown any benefit. Some studies have shown that moderate hypothermia for up to 48 hours, followed by slow rewarming, has prevented rebound intracranial hypertension as well as decreased ICP, however, there have not been any confirmed functional outcomes or decreased mortality rates benefits of this method (Adelson et al., 2013; Hutchinson et al., 2008).

Glycaemic control

Persistent hyperglycaemia (glucose > 10 mmol/L) should be treated. Hypoglycaemia (< 4 mmol/L) is much more dangerous. Persistent hyperglycaemia can be managed by reducing the dextrose concentration in IVF (which is usually administered in the first 48 hours of ICU care), or by starting an insulin drip.

A comment on imaging methods

In the UK, the initial investigation choice for detecting acute brain injuries is a CT head scan. A CT scan should be done within an hour of suspected head injury.
If there are no indications for a CT head scan (i.e. the signs/symptoms listed previously), a CT head scan should be performed within 8 hours of injury (NICE, 2014).

MRI scans are not usually done as the initial investigation, however, they have shown to provide information on the patient’s prognosis.

A final and most important note:

Don’t ever forget Safeguarding in children. Unfortunately, child maltreatment is common and can present anywhere. Have a look at the NICE guidelines below for more on how to identify child maltreatment.

Further reading

References

  • Adelson PD, Wisniewski SR, Beca J, Brown SD, Bell M, Muizelaar JP, Okada P, Beers SR, Balasubramani GK, Hirtz D; Paediatric Traumatic Brain Injury Consortium. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised controlled trial. Lancet Neurol. 2013 Jun;12(6):546-53. doi: 10.1016/S1474-4422(13)70077-2.
  • Araki T, Yokota H, Morita A. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurol Med Chir (Tokyo). 2017;57(2):82-93. doi:10.2176/nmc.ra.2016-0191
  • Finnegan R, Kehoe J, McMahon O, Donoghue V, Crimmins D, Caird J, Murphy J. Primary External Ventricular Drains in the Management of Open Myelomeningocele Repairs in the Neonatal Setting in Ireland. Ir Med J. 2019 May 9;112(5):930.
  • Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39(5):1093-1125. doi:10.1016/s0031-3955(16)38409-7
  • Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW; Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group. Hypothermia therapy after traumatic brain injury in children. N Engl J Med. 2008 Jun 5;358(23):2447-56. doi: 10.1056/NEJMoa0706930.
  • Kochanek PM, Tasker RC, Bell MJ, Adelson PD, Carney N, Vavilala MS, Selden NR, Bratton SL, Grant GA, Kissoon N, Reuter-Rice KE, Wainwright MS. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019 Mar;20(3):269-279. doi: 10.1097/PCC.0000000000001737.
  • National Institute for Health and Care Excellence. Head injury: assessment and early management. 2014. Available at: https://www.nice.org.uk/guidance/cg176
  • Ness-Cochinwala M., Dwarakanathan D. Protecting #1 – Neuroprotective Strategies For Traumatic Brain Injury. Paediatric FOAMed. 2019. 
Cite this article as: Nadine Schottler, Great Britain, "Immediate Management of Paediatric Traumatic Brain Injury," in International Emergency Medicine Education Project, November 16, 2020, https://iem-student.org/2020/11/16/paediatric-traumatic-brain-injury/, date accessed: November 24, 2020

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