Over the next few posts we are going to tackle head trauma, starting with some basic pathophysiology, determining a prognosis and then covering the principles of management.
The injury sustained by the brain is divided into two types or phases: primary and secondary.
Primary brain injury refers to the immediate injury sustained as a result of the traumatic event, for example, bleeding, bruising or laceration of brain tissue.
Secondary brain injury refers to the ongoing injury that occurs over a period of time after the primary insult. This is due to the secondary inflammatory changes, release of excitatory neurotransmitters and alterations in the cellular membrane permeability – all of which ultimately worsen the situation, leading to further destruction of brain tissue.
Coma scale
The Modified Glascow Coma Scale is a useful tool that enables a more objective grading and then serial monitoring of a patient’s neurological status. It can also help provide information regarding prognosis, as it has been demonstrated to have a linear correlation between the score and the survival rates of dogs with head trauma. An important point to remember is that the score can change rapidly once head trauma management has been instituted so repeat assessments every 6 to 8 hours is important.
The management of head trauma is mostly focused on maintaining cerebral blood flow. Cerebral blood flow is dependent on cerebral perfusion pressure (CPP), which is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP), which is what it is pushing against.
CPP = MAP – ICP
If the ICP is greater than the MAP, then there is no cerebral blood flow and no cerebral perfusion. Therefore, the ultimate goal of head trauma management is optimising CPP, as ischaemia develops without it, resulting in death of brain tissue. This, in turn, leads to further inflammation and further brain swelling and increased intracranial pressure.
Optimising MAP
Generally, efforts are directed towards optimising MAP, as this is what is driving oxygenated blood to the brain. This involves correction of perfusion deficits, which in trauma patients is most commonly caused by hypovolaemia from bleeding. Bleeding into cavities or bruising into tissues, common in polytrauma cases.
I almost always start replacing intravascular volume with a crystalloid. Normally, I would pick a isotonic buffered crystalloid, but in these cases I use 0.9% saline, as the higher level of sodium can help have additional benefits with traumatic brain injury.
I administer the fluids as 10ml/kg to 20ml/kg boluses over 5 to 10 minutes and reassess the patient’s perfusion parameters, for example, heart rate, capillary refill time, gum colour, pulse quality and blood pressure and body temperature, lactate and blood pressure. I aim to restore normal blood volume and blood pressure (MAP >70mmHg), but if I get to 30ml/kg to 40ml/kg of crystalloid and the patient is not stabilising, I start to think about why, for example is there continued internal bleeding?
If so, can I stop the bleeding and should I consider blood products to minimise the effects of haemodilution. If the patient is not dehydrated, I would consider hypertonic saline 7% to assist with volume expansion; it also has several other beneficial effects, which will be covered in the third part of this series.
If there is no internal bleeding, I consider vasopressor therapy, such as a dopamine CRI, to assist with in increasing mean arterial pressure.
The next post we will cover the management of Intracranial pressure…
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