Brad Gander is a Paramedic working in Brighton. Brad has an interest in critical care and wrote the following blog piece as part of our #AirwayWeek. Tweet Brad @BG_999 and let him know what you think!
As part of airway week I thought it would be good to review an article published earlier this year in Resuscitation entitled ‘Impact Brain Apnoea – A Forgotten Cause of Cardiovascular Collapse in Trauma’ (1). I found this article thought-provoking and feel it should be read by all pre-hospital clinicians for two reasons. Firstly, it reinforces the fact that prompt effective airway management and oxygenation is of paramount importance in the management of unconscious trauma patients. Secondly, clinicians infrequently witness the phenomenon of ‘Impact Brain Apnoea’ as it occurs in the immediate phase following injury, usually before pre-hospital services arrive. Awareness of the condition and circumstances in which it occurs may help improve recognition and subsequent management of these patients.
What is ‘Impact Brain Apnoea?’
Impact Brain Apnoea (IBA) is described as ‘the cessation of breathing after traumatic brain injury.’ The article notes IBA is most commonly described in motorcycle racing, and military environments as a result of blast injuries. This is because in these two contexts it is likely a clinician will reach the patient within the first few minutes of injury and witness the apnoeic phase. IBA differs from airway obstruction as a result of unconsciousness as it requires more than airway manouevres to reverse. Artificial ventilation alongside airway management will be required in order to prevent patients progressing into cardiac arrest as a result of hypoxia.
Why does it occur?
The article does not propose a definitive reason behind why IBA occurs however does discuss a number of historical accounts and animal studies that have described the phenomena. The majority of these accounts discuss cases in which patients with apparent TBI have been found to have little parenchymal injury at post mortem. This has led to a number of theories ranging from the brain being ‘thrown into a state of vibration temporarily suspending function’ (2) to ‘anaemia of the brain’ (3).
Radiological findings are discussed and it is noted that whilst microhaemorrhages demonstrated on MRI and CT imagery may be, and often are, attributed to diffuse axonal injury, these can also occur as a result of hypoxia (4). Due to this emphasis is placed upon assessment of the mechanism of injury and pre-hospital events when assessing patients found to have this pathology with little evidence of parenchymal injury.
A number of animal studies are summarised within the article and demonstrate incidence of IBA across a number of different animals injured via a variety of mechanisms. The majority of these studies found a link between the level of energy transfer and duration of apnoeic period.
Alongside the apnoeic phase seen in traumatic brain injury (TBI) a catecholamine surge also occurs, a great article by Atkinson (5) describes this in detail (see image below). This stress response elevates adrenaline and noradrenaline levels and creates subsequent hypertensive effects. When this is instilled upon a heart suffering from the effects of hypoxia cardiovascular collapse can occur and progress rapidly to cardiac arrest.
How will patients with IBA present?
IBA is thought to occur within the first 10 minutes of TBI, following injuries sustained as a result of high energy blasts and direct head trauma. Patients with IBA will present as unconscious with respiratory arrest, and may appear ‘shocked’ as a result of hypoxia and catecholamine induced cardiovascular collapse. The authors noted hypotension is relatively common following traumatic brain injury (6) and the potential to attribute these symptoms to haemorrhage, rather than acute brain injury and hypoxia, could delay meaningful interventions for patients with IBA.
How should we manage patients with IBA?
In cases of suspected IBA, when a patient with suspected TBI is found to be in respiratory arrest within the ‘critical phase’ (defined as 10 minutes post TBI), attention should be paid to providing early artificial ventilation alongside airway management manouevres. As observed by the authors of this article, and the findings of the documented case studies, ventilation during this period may be beneficial and lead to full recovery. This article highlights that apparent cardiovascular collapse in trauma may not necessarily always be a result of hypovolaemia. The optimal form of airway management is not discussed within this article, although the case reports included describe two cases in which simple airway manouevres (jaw thrust) and ventilation via mouth-to-mouth resuscitation or bag-valve-mask resulted in a return of spontaneous respiratory effort and good neurological recovery.
What does the future hold?
The authors suggest future TBI research is focused upon the immediate minutes following injury in order to investigate this phenomenon further and provide insight on how we can intervene during this critical period of care. We already know the principles of prompt recognition, swift community response and basic life support procedures are demonstrated to improve outcomes from cardiac arrest, is it now the time to apply these to IBA? In these cases, rapidly performed airway manouevres accompanied with effective ventilation represent a simple treatment capable of achieving good outcomes in patients with time-critical neurotrauma.