Severe head injuries: Neuroprotection

Severe head injuries: Neuroprotection

35yo female fallen from a first floor window onto a concrete hard standing. She was witnessed to fall and land head first! She is unresponsive, hyperventilating with markedly increased respiratory effort. There is an obvious head injury but there are no other apparent injuries.

For those of you working in pre-hospital care, the term neuroprotection is frequently banded around when the subject of head injury emerges. But what does neuroprotection mean for the pre- hospital management of the head injured, and why make a deal of it.

This week I’ll be outlining the emergency management of severe head injuries (ill focus on isolated head injury for this one) and how as pre- hospital clinicians, we can reduce the impact of secondary brain injury. Incidentally I’ve just written about this very subject as part of my MSc but ill rid this post of any academic chat.

Primary brain injury is the caused by the initial insult. It has already happened so there is nothing that we can do about it. What we can change, is the brain injury that occurs secondary to this as a result of cerebral hypoxia. Hypoxaemia, hypercapnia, hypoglycaemia, hypotension and raised intracranial hypertension will all have a detrimental effect. Even isolated head injuries, if severe enough will cause respiratory and haemodynamic instability and will be worsened further still if other injuries are present.

The ideal scenario is that a pre-hospital advanced care team rock up in orange and anaesthetise your patient on scene like super hero, but in reality you will usually need to manage and transfer these without senior input. Whilst emergency anaesthesia (RSI or PHEA depending on local terminology) is the ideal treatment because enables more effective control of hypoxia, hypercapnia and ICP it isn’t always available in an acceptable time. Bearing in mind it will take a good 10-15mins for the patient to be prepared, anaesthetised and readied for transfer, so weigh this up against getting gone ASAP. E.g if you’re 10mins from a major trauma centre then clearly waiting for advanced care team might be detrimental, but if you’re an hour away and the team can get to scene or render vous in a short time, then the risk/ benefit balance shifts. If you think there may be a benefit to staying, then start getting the patient packed up and ‘phone a friend’ from your friendly local advanced care team for their experienced opinion. They can always meet en route to offer support and intervention if required.

The table below outlines the potential indications for immediate RSI of the head injured patient (if expertise are available).

So. What can we do without RSI capability at our disposal?

The Guidelines from the Association of Anaesthetists and the Neuro Anaesthesia and Critical Care Society are a must read. Although they relate to inter-hospital transfer, many of the principles are equally applicable to pre-hospital emergency care.

Respiratory management-

High quality airway management is a must and needs to be as good as it can be as soon as possible because this is the biggest cause of hypoxaemia in this group. It is worth noting that tracheal intubation will often provoke a sympathetic response that drives up heart rate and blood pressure, so ideally needs to be achieved under anaesthesia.

Oxygen titrated to achieve reliable saturations of >94% or if you’re really Gucci then achieving a normal PaO2.

If you’re ventilating the patient aim to get their EtCO2 somewhere between 4.5- 5.0Kpa (4- 4.5kpa if at risk of impending herniation). There is a fairly good correlation between EtCO2 and PaCO2 UNLESS significant chest injury also present.

Beware of spontaneous pneumothorax in the positive pressure ventilated patient and have a low(ish) threshold for intervening with either needle decompression or finger thoracostomy.

Circulatory management

Blood pressure management will depend on whether there is an isolated head injury, or whether the patient is multiply injured. The latter will usually have blood pressure maintained to palpable pulses (for the first hour then near normal blood pressure should be aimed for there after).

Prevent or address hypovolaemia by splinting long bone and pelvic fractures, tamponade external haemorrhage and cautious use of cold water infusions (i.e. 0.9% Saline). If isolated head injury, then cold water or inotropic drugs can be used to get BP to target (see table below).

Intracranial pressure- 

Rigid neck collars are the devils work, especially in brain injuries. Not only do they impede airway management, they restrict venous return from the head and so contribute to raising the ICP. When immobilising the spine this is ideally done with head blocks and taping the forehead but avoid taping across chin/ neck as it will restrict airway management and might compress the neck vessels.

Adopt a slightly head up position on the ambulance trolley, somewhere between 20-30degrees. There is no clear evidence of the ideal degree of tilt so I wouldn’t get too het up if you forget to take your protractor to work! What is important is that their head is higher than their feet.

One other thing, don’t let Colin McRae drive the ambulance! Firstly because you’d like to stay in your seat, secondly you need to be able to treat the patient in the back without being subjected to 10G under braking and acceleration, but there is some evidence (albeit not strong) that linear and lateral G-forces will transiently affect ICP and blood pressure, so a smooth drive without harsh acceleration/ braking might help (the patient). It isn’t clear what the impact of transient changes in BP/ ICP has on outcomes though.

What else?

Keep them warm too. Remember the triad of death- hypothermia, hypovolaemia and DIC- i.e. widespread clotting fury unleashed.

Have an anticonvulsant handy too (most commonly Diazemuls in UK pre-hospital practice but there will be a move away from this in the near future) and don’t be afraid to use it! Seizures worsen hypoxia, elevate blood pressure and therefore ICP so need stopping ASAP. The worse that happens is that they become respiratory depressed or apnoeic, which to my mind makes the patient easier to manage, since you’ll have control of ventilation guided by EtCO2 and SpO2. NB I’m not for 1 minute suggesting that we accidentally on purpose sedate/ anaesthetise the head injured patient. I am simply trying to offer reassurance that the worse case scenario of Diazemuls induced apnoea isn’t actually that bad! You’d need to report it as an unintended medicine related incident, but if your airway and ventilatory management is spot on, there shouldn’t be any dramas.

The final thing to consider is the destination. Head injured patients will benefit from being transferred directly to a specialist neurosciences centre (most major trauma centres will be geared up to manage these patients). We know that patients requiring secondary transfer to a neuro centres are significantly more likely to have poorer outcomes. This was part of the reason that major trauma networks were implemented.

Sources – 

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