An 8 year old boy is rushed into ED following a fall from a fourth story window. Â He landed on concrete and has obvious signs of external damage to his skull and a GCS of 5.He’s clearly sustained a serious traumatic brain injury – how is this best managed?
Severe traumatic brain injury (TBI) is typically defined by an initial GCS score of ≤ 8.
How common is it?
In Australia, admission rates for paediatric TBI is 91.1 per 100,000, with 34.7 per 100,000 resulting in a high threat to life (data collected 2000-2006)1. Remote-dwelling children are disproportionately represented amongst this group.
What’s the pathophysiology?
TBI is a dynamic process consisting of the primary injury followed by secondary brain injury due to a combination of systemic derangements (eg. hypoxia, hypotension, hypercarbia) and local events (eg. herniation, compression)2. Glutamate-mediated excitotoxic effects, oxidative stress, inflammation, ion imbalance, and metabolic abnormalities combine to cause progressive neuronal necrosis and apoptosis2.
How is it best managed?
Needless to say that ABC is always your first priority as this patient has a GCS of 5.
The aim of hospital management of severe TBI is to limit secondary brain injury.
The most frequent cause of death and disability after severe TBI is intracranial hypertension. Management of intracranial hypertension, in order to maintain adequate cerebral perfusion pressure, is central to neurocritical care of children after severe TBI.
Observational studies show that ICP monitor-based management of intracranial hypertension in severe TBI is associated with improved survival and neurologic outcome.3
Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)
The traditional threshold for intracranial hypertension is 20mmHg (for ≥ 5 minutes), however this is based largely on adult studies. Some studies suggest children have less autoregulatory reserve and therefore should have lower ICP thresholds.3
Neuroimaging
Early CT scan allows rapid detection of intracranial injury (up to 75% of severe TBI) and facilitates prompt neurosurgical intervention.
Subsequent CT scans are considered for further neurologic deterioration or increasing ICP.
The role of MRI is not yet established.Â
Hypothermia
Animal models and adult studies correlate hyperthermia with worse outcome, as it augments the pathophysiological response after injury.
The suggested role for hypothermia is through a reduction in cerebral metabolic demand, inflammation, lipid peroxidation, excitotoxicity, cell death, and seizures.
However, paediatric data remains inconclusive due to discrepancies in optimal timing of onset and duration, rate of rewarming, and standard practice amongst studies.
Adverse effects of hypothermia include clotting disturbance, increased risk of infection, cardiac dysrhythmias, and insulin resistance.Â
Hyperosmolar therapy
Despite the longstanding clinical acceptance of mannitol, there remains a lack of evidence to support its efficacy in reducing ICP.3Â There is more promising evidence to support the use of hypertonic saline.3Â Optimal osmolar levels have not been determined.Â
Hyperventilation
This results in hypocapnia-induced vasoconstriction, leading to a reduction in cerebral blood flow and volume, thereby reducing ICP. It is commonly employed despite a lack of evidence.3Â
Corticosteroids
Are considered to restore altered vascular permeability, reduced oedema and CSF production, and decrease production of free radicals.
A few studies demonstrate no improvement in ICP, functional outcome, or mortality.3Â
CSF drainage
The rationale for CSF drainage is to reduce intracranial fluid volume and therefore ICP. This may be achieved through an external ventricular drain (EVD) and/or a lumbar drain.
There are no randomised control trials to establish efficacy3; however CSF drainage is considered when intracranial hypertension proves refractory to non-surgical measures.Â
Analgesia, sedation, paralysis
This limits pain and stress which can contribute to increased metabolic demands, cerebral blood volume, and ICP.
It can cause cardiovascular instability, leading to reduced mean arterial pressure and cerebral perfusion pressure. Choice of agents remains up to clinical experience.Â
High dose barbituates
These improve coupling of regional blood flow and metabolic demand by suppressing cerebral metabolism and altering vascular tone. This limits oxidative stress and excitoxicity.
There is limited evidence to suggest the efficacy of high dose barbituates as an adjunct to reducing ICP, with no established benefit on survival or neurologic outcome.3
Cardiorespiratory adverse effects are common.Â
Anticonvulsant prophylaxis
The incidence of early post-traumatic (< 7 days) seizures is approximately 10%.
Prophylactic phenytoin reduces the incidence of early post-traumatic seizures; however there is no conclusive data to suggest a role for phenytoin in preventing long-term post-traumatic seizures or improving neurologic outcome.3Â
Decompressive craniectomy
The evidence base – largely from observational studies – demonstrates efficacy in treating intracranial hypertension refractory to non-surgical management, which correlates with improved outcome.3
One paediatric randomised control trial (Taylor 2001) demonstrated a non-significant reduction in ICP at 48 hours, but a significant improvement in 6 month outcome associated with early decompressive craniectomy.Â
References
- Berry JG, Jamieson LM, Harrison JE. Head and traumatic brain injuries among Australian children, July 2000 – June 2006. Injury Prevention, 2010; 16: 198-202.
- Rosenfeld JV, Maas AI, Bragge P, et al. Early management of severe traumatic brain injury. Lancet, 2012; 380: 1088-98.
- Kochanek PM, et al. Guidelines for the acute management of severe traumatic brain injury in infants, children, and adolescents – second edition. Paediatric Critical Care Medicine, 13(1) Suppl.
- Taylor A, Butt W, Rosenfeld J, et al. A randomised trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Child’s Nervous System, 2001; 17: 154-162.
