If Grey’s Anatomy has taught us anything, it is to assess for secondary brain injury following ANY head injury! Things could have gone so differently for our favourite McDreamy neurosurgeon…
It is important to acknowledge that however bad a primary brain injury might be, it is the secondary brain injury that kills the person. So what is the difference between primary and secondary brain injury? Primary brain injury occurs during the initial insult; someone falling from a ladder and hitting their head on the ground for instance. It may result in a contusion, damage to blood vessels and/or axonal shearing. Secondary brain injury is what occurs as a result of the primary injury secondary to the pathophysiological process of inflammation within the brain.
Before moving on to the pathophysiology of secondary brain injury, it is important to understand a few key concepts and definitions.
- Even though the brain is squishy, the skull that contains it is not – it is a fixed vault that does not allow any expansion past its rigid constraints
- The brain vault contains brain tissue, cerebral spinal fluid (CSF) and blood (both arterial and venous)
- These three components within the brain vault make up a fixed internal volume that maintains a state of equilibrium that achieves a normal intracranial pressure (ICP)
- Therefore, any increase in one of these components within the brain vault will have to result in a compensatory decrease in another component within the brain vault in order to maintain a state of equilibrium that achieves a normal ICP
- If an increase in one of these components within the brain vault does not have a sufficient compensatory decrease in another component within the brain vault, an increase in ICP will occur
- This is known as the MONROE KELLIE HYPOTHESIS
The brain tissue that accounts for 80% of the space within the brain vault has a limited ability to compensate. Therefore, it is the blood and CSF that needs to be displaced out of the brain vault to maintain equilibrium. Each of these components account for 10% of the space within the brain vault and can only be compensated to a certain physiological limit. A reduction in arterial blood will result in cerebral ischaemia, so it is mainly the venous blood that is displaced during compensation. CSF is either displaced downward into the spinal sub-arachnoid space or it experiences a decrease in production or an increase in reabsorption during compensation.
This is all done to maintain a normal ICP of between 7 – 15 mmHg in the supine person or 0 – 10 mmHg in the person with an elevated head. Any ICP that is greater than 20 mmHg is referred to as a pathological ICP as this is the point that can start to cause some serious consequences for the person. This is because the higher the ICP gets, the more resistance the mean arterial pressure (MAP) in the body has to face in order to get oxygenated blood from the heart into the brain for perfusion. The normal range for MAP is approximately 60 – 100 mmHg. MAP and ICP are the two factors that impact cerebral perfusion pressure (CPP), which is the pressure required to ensure adequate perfusion of the brain. The CPP needs to be greater than 50 – 60 mmHg to ensure adequate cerebral perfusion, with the normal range being approximately 60 – 150 mmHg.
In order to calculate MAP and calculate CPP, use the following formulas:
MAP = Systolic BP + (Diastolic BP x 2)
CPP = MAP – ICP
By understanding the relationship between ICP, MAP and CPP; it is clear to see why an ICP greater than 20 mmHg can be pathological. If the person has a MAP of 60 mmHg with an ICP of 20 mmHg, their CPP would only be 40 mmHg. This is insufficient to sustain adequate cerebral perfusion and cerebral ischaemia will ensue. The flow chart below explains the pathophysiology of secondary brain injury and how it can eventually lead to brain death, which we actively try to avoid!
As discussed above, increased ICP can be compensated for in three ways:
- Increasing the MAP as the ICP increases to ensure adequate CPP
- Decreasing the venous blood within the brain vault to reduce ICP
- Decreasing the CSF within the brain vault to reduce ICP
These three methods are the cornerstone of managing increased ICP in a hospital setting while allowing time for the primary injury to be rectified. During this time, it is recommended that the metabolic demands of the brain is kept as low as possible. To achieve all of these interventions in order to prevent decompensation, these patients are often managed in an intensive care unit. The following mnemonic can be utilised to remember the interventions required when managing patients with secondary brain injury: ACTS For Preventing Secondary Brain Damage!
Angle head of the bed ≥ 30 degrees
- This facilitates easier displacement of venous cerebral blood into the systemic system and cerebral CSF into the spinal region via gravity drainage
- It is important to ensure that the head of the patient does not tilt to one side, thereby blocking effective drainage of venous blood
- There are many causes that can result in increased ICP including:
- Oedema and swelling that requires time to decrease
- Intracranial haemorrhage that requires immediate surgical evacuation if it is large or time to reabsorb if it is smaller
- Brain tumour that requires surgical intervention to remove, if possible
- Maintain temperature between 35 – 37 degrees to reduce cerebral metabolic demands
- Increased ICP can lead to an increased risk of seizures
- Seizures further increase ICP and cerebral metabolic demands and therefore should be actively prevented, if possible
Fluid status and electrolytes
- Maintain even balance for the patient and ensure that electrolytes are within their normal ranges
- If intravascular filling is required, colloids should be avoided due to studies showing an increased mortality when used in patients with neurological pathophysiology
- Cerebral oedema can be reduced by utilising Mannitol to shift fluid from the intracellular cerebral tissue into the intravascular space, which can then be removed from the body by utilising a diuretic such as Frusemide
Perfusion and pressures
- Maintain the following pressures within the body:
- MAP ≥ 60
- ICP ≤ 20
- CPP ≥ 60
Sedation and analgesia
- This reduces the increased ICP and cerebral metabolic demands associated with increased levels of consciousness/anxiety/pain/endotracheal tube intolerance etc
- Ensure the patient is disturbed as little as possible and that all interventions potentially increasing cerebral metabolic demands are grouped together
- Maintain carbon dioxide levels between 30 – 40 mmHg in order to reduce the cerebral vasodilation associated with hypercapnia
- By avoiding excessive cerebral vasodilation, cerebral venous blood will be more easily displaced as it will not pool within the brain vault
- Maintain partial pressures of oxygen (PaO2) ≥ 60 to ensure adequate oxygenation to aid with cerebral perfusion
- If the pathophysiological process of the secondary brain injury is too severe, additional interventions may be required to help with compensation:
- The insertion of an external ventricular drain (EVD) via a ventriculostomy to help drain excess CSF from the brain vault and additionally monitor ICP
- A craniotomy to remove a portion of the skull to allow for excessive swelling of brain tissue
What are your experiences with managing a patient with secondary brain injury? Does your facility have a policy for the management of patients that have sustained a strike to the head? Is your facility utilising different methods to what is listed above when managing a patient with a secondary brain injury? Please feel free to leave your comments or ask any questions in the section below…
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