One-liner…
Understanding the underpinning principles and management of raised intracranial pressure is essential for reducing the morbidity and mortality of traumatic brain injuries.
Seven-year-old Dan was involved in a motor vehicle collision.
At the scene, he was vomiting and drowsy with a low Glasgow Coma Score (GCS). The air ambulance service intubated him at the scene and pre-alerted the department before arrival.
Traumatic brain injury (TBI) is a major cause of death and permanent disability in children and young people. It occurs when a mechanical force to the head injures the brain. This can be from the brain hitting the skull, shear forces from sudden acceleration and deceleration, or direct injury at the point of impact.
The severity of head injuries can be classified according to the GCS. Children and young people with a GCS of 8 or less are classified as having a severe TBI, and this is associated with significant morbidity and the highest rates of mortality.
Understanding the natural history of brain injuries can help us visualize the underlying pathological process and how treatments can focus on reducing raised intracranial pressure (ICP) and protecting the brain.
TBI occurs in two stages: a primary brain injury and a secondary brain injury.
The primary brain injury is direct damage to the brain from the trauma itself. This is immediate and can be just in one place (focal) or affect the whole brain (diffuse), with damage occurring to brain tissues, blood vessels, neurons, and other surrounding structures. This insult to the brain is often irreversible.
In secondary brain injury, the initial injury triggers a range of inflammatory and neurotoxic responses, which causes further progressive injury to the brain. The mechanism is complex, involving oedema, hypoperfusion, hypoxia, ischaemia, hyperexcitement of neurons and release of chemicals and reactive oxygen species, which further damage the neurons. This secondary injury occurs shortly after the primary injury and can progress days after the initial trauma. Treatments and measures to protect the brain are important to try and limit the impact of this secondary brain injury.
How does raised intracranial pressure occur?
Raised ICP plays a key role in developing secondary brain injury, and understanding the basic anatomy of the skull and its contents can help us understand this process.
When the fontanelles fuse, the skull becomes a vault that can only house a fixed volume. This vault contains the brain, blood, and cerebrospinal fluid (CSF). The Monro-Kellie Doctrine describes how intracranial pressure (ICP) is determined by the relationship between these three components within a fixed cranium volume. When the volume of one of these components increases (e.g., the brain if there is oedema due to cellular injury and tissue ischaemia), the intracranial pressure will also rise.
Following a traumatic brain injury, intracranial pressure can increase for several reasons.
Bleeding and haematoma
Bleeding and haematoma formation can be anatomically related to the injured vessel, for example, extradural, subdural, or subarachnoid haemorrhage, or directly from bleeding or bruising within the brain (intraparenchymal bleeding or contusion). This can cause a direct mass effect on the brain tissue and further worsen blood supply, ischaemia, and the resulting damage.
Impaired cerebral autoregulation
The regulation of the circulation around the brain is finely balanced to provide a continuous supply of oxygen and nutrients to the areas of the brain that require them most. These autoregulatory mechanisms are impaired after TBI, disrupting this fine balance and can cause cerebral ischaemia or oedema with changes in systemic blood pressure. Oxygen and carbon dioxide levels are targeted clinically to optimise cerebral blood flow by their effect on cerebral vascular reactivity.
Impaired venous drainage
Impaired venous drainage increases the venous blood mass, which can lead to blood pooling in the intracranial compartment and further raise the ICP.
Additionally, increased intrathoracic pressure can slow venous drainage (as overall venous pressure increases). This can be caused by high mean airway pressure due to mechanical ventilation, tension pneumothorax, large haemothorax, cardiac tamponade, and even due to straining from distress.
Impaired CSF drainage
CSF drainage can be obstructed due to compression of the CSF circulation by surrounding oedema or haematoma, anatomical injury to the drainage system, or drainage system blockage by turbid blood or CSF. Impaired CSF drainage increases the volume of CSF, causing acute hydrocephalus and a rise in ICP.
Cellular swelling
Oedema can occur for numerous reasons. These include direct cell damage and the local inflammatory response to cellular damage.
Increased intracranial pressure itself can lead to a vicious cycle of increasing damage to the brain. The raised pressure can cause direct cellular injury, leading to further tissue oedema, impaired perfusion, and rapidly increasing pressure. As such, minimising the impact of this process is crucial.
What neuroprotective measures can we undertake in the emergency department?
After a traumatic brain injury, all children and young people should have a C-ABCDE rapid assessment for life-threatening injuries (as per ATLS guidelines) focussed on trauma resuscitation and stabilisation, followed by a secondary assessment. Ideally, all patients with severe TBI should be managed in trauma centres with expertise in neurosurgical and intensive care management.
Neuroprotective measures are undertaken in the emergency department and PICU to optimise intracerebral conditions, minimise secondary brain injury, and create optimal tissue healing conditions.
The most widely used guidelines are the Brain Trauma Foundation Management of Paediatric Severe Brain Injury guidelines, although local centres may have variations on this. These guidelines detail neuroprotective strategies with supporting evidence. In general, a neuroprotective strategy subscribes to the following basic principles:
Avoiding increased intracranial pressure
This involves avoiding hyper- or hypocarbia, hypoxia, acidaemia, obstructed venous drainage, or thoracoabdominal muscle contraction during straining (which results in increased central venous pressure). Children should also be nursed in a neutral position and have the head end elevated by 15-30 degrees to improve venous drainage.
Maintaining cerebral perfusion pressure
Adequate brain perfusion depends on the driving pressure of blood entering the cranial vault—the cerebral perfusion pressure (CPP).
The CPP is derived from the mean arterial and intracranial pressure (CPP= MAP-ICP) targeting normal CO2, avoiding hyper- and hypotension, and measures to reduce ICP.
Reducing cerebral metabolic demand
Decreasing cerebral metabolic oxygen demand using deep sedation theoretically reduces the metabolic stress and demand from the brain. This may involve prophylactic anticonvulsants, avoiding low or excessively high glucose levels, avoiding fever and maintaining a normal temperature. There is weak evidence to suggest that moderate hypothermia (32-33oC) can be used for ICP control in specialist settings.
All children and young people with severe TBI require endotracheal intubation for airway control.
Oxygenation and ventilation should be continuously measured with pulse oximetry and end-tidal CO2 monitoring. Arterial oxygen levels should be maintained above 11 kPa, and hyperoxia should be avoided. The arterial carbon dioxide should be maintained between 4.5-5 kPa since changes in CO2 can lead to changes in cerebral blood flow. Low CO2 causes cerebral vasoconstriction, which can lead to cellular hypoperfusion and cerebral ischaemia, whilst a high CO2 can lead to vasodilation, which can increase blood flow to the brain and, therefore, increase blood volume and intracranial pressure.
Sedation and neuromuscular paralysis are recommended. For sedation, a combination of benzodiazepines and opioids is often used. These should be carefully titrated to avoid hypotension. Neuromuscular paralysis helps to reduce intrathoracic pressure, which improves venous return. It also prevents shivering and posturing, therefore reducing the cerebral metabolic demand.
Circulatory support is crucial for preventing both hypotension, which can lead to brain ischaemia and hypertension. This can worsen oedema and raise ICP.
It has been shown that even a single episode of hypotension dramatically increases mortality. Isotonic fluids are recommended to prevent hypotension, whilst fluid boluses and vasoactive agents may be required to aggressively treat any hypotensive episodes.
What about hyperosmolar therapy?
Hyperosmolar therapy has long been a cornerstone in the management of paediatric TBI. Increasing the osmolarity of the blood creates an osmotic gradient that allows fluid from outside the blood vessel to enter the blood vessel and, therefore, reduces brain oedema.
Mannitol and hypertonic saline are the two most used hyperosmolar therapies.
Mannitol is a sugary fluid that can be given in 1 to 2g/kg body weight boluses over 30 minutes to an hour to reduce ICP. Mannitol stays solely in the blood vessels, so it doesn’t cause electrolyte movements into the brain tissues. Only a small amount of mannitol is reabsorbed by the body. The osmolarity is also increased in the kidneys, which leads to diuresis. Hence, it’s important to monitor blood pressure to avoid any episodes of hypotension after mannitol.
Hypertonic saline contains a higher sodium concentration than normal plasma and interstitial fluid. This drives the osmotic gradient and helps reduce cerebral oedema. In children and young people with TBI, 2 – 5mL/kg boluses of 3% hypertonic saline at 10-minute intervals are recommended. A continuous infusion of 3% saline between 0.1 and 1.0 mL/kg per hour on a sliding scale can also be used in the PICU setting with careful electrolyte and osmolarity monitoring. Hypertonic saline increases serum sodium and has less of a diuretic effect than mannitol. This is likely due to the increased serum sodium causing the release of anti-diuretic hormone. There are fewer issues with fluid balance and blood pressure management.
There is some evidence to support hypertonic saline as the therapy of choice for raised ICP.
Do we need seizure prophylaxis?
Children and young people have lower seizure thresholds than adults. Following TBI, seizures are common and may be missed in children and young people who are sedated and paralysed.
Prophylactic anticonvulsants should be started early to reduce the risk of post-traumatic seizures, which can rapidly increase the cerebral metabolic demand. Either levetiracetam or phenytoin can be used for seizure prophylaxis.
Take-home messages
Knowing how and why raised intracranial pressure occurs can help apply clinically relevant treatments.
Neuroprotective strategies should be initiated as soon as possible in the emergency department and continued further in the PICU.
Neuroprotective strategies aim to avoid increased intracranial pressure, maintain cerebral perfusion pressure, and reduce cerebral metabolic demand.
About PICSTAR
PICSTAR is a trainee-led research network open to all doctors, nurses and allied health trainees within Paediatric Intensive Care. We are the trainee arm of the Paediatric Critical Care Society – Study Group (PCCS-SG) and work with them on research, audit and service evaluation.
If you would like to join PICSTAR and get involved in projects, have ideas you would like to propose or get advice/mentorship via PCCS-SG, don’t hesitate to contact us at picstar.network@gmail.com. See their website for more: https://pccsociety.uk/research/picstar/
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