Learning Objectives

impact brain apnoea



Explore the epidemiology behind traumatic brain injuries in our community.


Refresh the pathophysiology of traumatic brain injuries, and how they relate to pre-hospital practice.


Define and understand Impact Brain Apnoea and its relevance to prehospital clinicians.


Identify the implications on our practice and considerations for care. Importance on early recognition and correction.

Alexander Spanos

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what is a traumatic brain injury?

The terms "head injury" and "traumatic brain injury" are sometimes used interchangeably, however it is important to understand the differences between them.

Head injuries are a broad classification that encompass an array of injuries to the head. This includes injuries to the scalp, skull, brain and underlying tissues and blood vessels. [1] Essentially, it is any form of trauma to the head regardless of neurological function. [1]

Traumatic Brain Injuries (TBIs) are complex injuries, with a broad spectrum of associated symptoms. They are defined as non-degenerative, non-congenital insults to the brain and brain function resulting from an external mechanical force. [2] They can lead to temporary and permanent alterations in cognitive, physical or psychosocial functions with the potential for focal neurological deficit or an altered conscious state. [2] [3]  


Traumatic Brain Injuries can be classified using the Glasgow Coma Scale (GCS): [3]

-          Mild TBI = GCS 13-15

-          Moderate TBI = GCS 9-12

-          Severe TBI = GCS <8


Traumatic Brain Injuries (TBIs) are among the most significant cause of death and disability following trauma. Severe TBIs only make up a small percentage of head injuries, however their social and economic impact is extensive. In Australia, TBI’s cost an estimated $184 million annually in hospital bills – in addition to this, those with longstanding disabilities may continue to require assistance for daily tasks indefinitely. [4]

Utilising data from the Victorian State Trauma Registry, the Australian Institute of Health and Welfare conducted a retrospective analysis investigating the incidence of severe TBI’s in Victoria over a period of 9 years (2006-2014). [4] Over the 9-year period, 2062 patients were identified as being hospitalised with severe TBI, which makes up 9% of total major trauma cases. [4] The average incidence of severe TBIs in Victoria is 4.2 cases per 100,000 population, per year. [4] The in-hospital mortality rate of the 2062 individuals in the analysis was calculated to be 42.5%. This was found to be significantly higher in those aged >65 with a mortality rate of 77.8%. [4]

Across all age groups, males have significantly higher rates of severe TBI when compared to females. The most affected age groups for both genders are young adults (15 – 25) and older adults (>65). [5]

The top 3 most common causes of TBI are: [4,5]

  1. Falls - 42.1%

  2. Transportation - 29.4%

  3. Intentional (inflicted by another person – assault) - 14.4%

Presently, data describing the incidence of mild/moderate TBI’s in Australia is scarce. Data extrapolated from national Emergency Department presentations in 2005-06 depicts approximately 22,710 presentations where the principle diagnosis was head injury. Furthermore, a total of 5925 presentations suggested head injury was an additional diagnosis. [5] Data involving number of ambulance attendances to these events was unable to be sourced, however it is evident from presentations to the Emergency Department that head injuries of all severity can make up a significant proportion of our pre-hospital workload.

Pathophysiology of traumatic brain injuries

Refresh your knowledge! Click on each box to learn more.



The first 10 minutes post head injury has been arbitrarily coined the “critical phase.” [50]

Impact Brain Apnoea (IBA) is one of two components that make up the critical phase of head injury. It has been postulated that Impact Brain Apnoea is a preventable cause of cardiovascular collapse in head injured patients. [50] [51]


So, what is it?

IBA describes a phenomenon where any concussive blow to the head results in a period of apnoea. [50] Recently, it has begun to gain traction again - Gareth Davies (among others such as the late Dr John Hinds), Medical Director of London's Air Ambulance Service, began to see the phenomenon whilst working in his role as Medical Director at the Isle of TT races (high speed motorcycle racing through the public streets of Ireland). [52] Due to the nature of his role, he would often see head injured patients immediately after injury - he noted the incidence of apnoea, and the seemingly remarkable recovery these patients had with early intervention. [51] [52]


Various studies have shown that the period of apnoea and degree of respiratory recovery is directly proportionate to the amount of force that has been exerted and transferred to the brainstem. [50] [51] The apnoea can range from a brief gasp to a prolonged, unrecoverable apnoeic period. [50] [51] Interestingly, these studies have also shown that subjects who died following this period of apnoea had little to no structural damage to the brain, contrary to what the researchers would have anticipated. [50] [51] Further studies demonstrated that basic interventions (i.e. opening the airway and providing assisted ventilations) can lead to a complete neurological recovery. [50] [51] Unfortunately, the mechanism remains poorly understood however appears to be brain-stem mediated due to its occurrence in prepared decerebrate animals. [50] [51]


What studies have been done?

Animal models of head injuries have shown the association between concussive forces and apnoea. [51] It has been demonstrated across several different species with varying mechanisms. Below are some key studies and a brief summary of their results:

Koch & Filehne, 1874 – Repeated blows to the head of a dog resulted in death by respiratory paralysis / apnoea, despite there being no apparent structural abnormality to the brain. [50] [51]

Polis, 1884 – Concussive head injury to cats, dogs and rabbits lead to death by respiratory paralysis despite no anatomical lesions [51] 

Miller, 1927 – Repeated Polis’ work with identical finding [51] 

Denny-Brown & Russell, 1941 – Clearly showed death from the experimental head injuries was due to respiratory paralysis. Using respirometry, they demonstrated that as the force exerted increased so did the period of apnoea. A light blow causes a gasp, a moderate blow had varying periods of apnoea / recovery, and a heavy blow caused prolonged apnoea and subsequent death via hypoxic cardiac arrest. Furthermore, they concluded that this reflex was brain stem mediated as it also occurred in decerebrate prepared animals.  Upon sectioning the brain, there were no lesions noted. [51] [53]

Walker et al, 1944 – Studied concussion in different animal species with a variety of mechanisms. As seen by Denny-Brown & Russell (1941), Walker et al also observed that the period of apnoea was dependent on the force exerted. Additionally, it was further established that this was mediated by the brain stem and independent of intracranial pressure. [50] [51]

Sullivan et al, 1976 – Using fluid percussion with cats, found that apnoea was produced with no structural damage to the brain. Interestingly, it was also noted that in animals where the fluid percussion exceeded the lethal force, early respiratory support lead to a complete recovery. [50] [51] [54]

Adelson, 1996 – Weights dropped onto rats’ heads demonstrated impact brain apnoea. Again, with respiratory intervention mortality was largely reduced. [51] [55]

Rafaels, 2011 and Rafaels, 2012 – Studied explosive blast waves and their effect on animals. Apnoea was noted in both studies, with the duration of apnoea proportionate to the blast force. [51] [56]

These studies demonstrate a few key points

  1. Impact Brain Apnoea occurs with ANY concussive force to the head

  2. The duration of apnoea and degree of respiratory recovery is directly proportionate to the amount of force exerted on the brain stem

  3. Death occurred without any structural damage to the brain

  4. With early intervention / respiratory support, complete neurological recovery is possible

the other component in the critical phase

The other aspect of the critical phase is catecholamine surge. [50]


Following a head injury, massive sympathetic discharge occurs with significant increases in arterial blood pressure and heart rate. [50] [51] It has been demonstrated that following significant head trauma, adrenaline levels increase by 500-fold, whilst noradrenaline levels increase by 100-fold. [50] [51] Although this is not directly related to Impact Brain Apnoea, it potentiates secondary injury by augmenting the hypercapnic cerebral vasodilation, promoting early vasogenic oedema. [50] In addition to this, it also results in blood brain barrier disruption, endothelial injury and may contribute to rises in intracranial pressure. Studies have demonstrated that this is a brain-stem mediated stress response following severe head injury. [50] [51] 

This component may explain hyperglycaemia, gastric ulcerations, myocardial injury and pulmonary oedema that occurs following a traumatic brain injury. [32] [37] [39] [50]


what Is the impact of impact brain apnoea?

As previously discussed, Impact Brain Apnoea is a very real contributor to morbidity and mortality in head injured patients. As pre-hospital clinicians, we have the opportunity to alter the trajectory of these patients and dramatically improve patient outcomes.

The nature of the prehospital environment is that it's dynamic and filled with endless possibilities.  Part of this is the possibility to witness and incident, or arrive within the critical period following an incident. Cardiovascular collapse in severe head injury may be attributed to Impact Brain Apnoea and intervention can lead to a full recovery - Impact Brain Apnoea may one day be considered another Reversible Cause of Cardiac Arrest in Trauma.


Through early recognition and appropriate interventions, we can save lives.

What happens if we don't intervene?

For the apnoeic patient that doesn't recover their respiratory drive, we can predict the outcome - death from hypoxic cardiac arrest. However, what about those that do recover their respiratory drive? Without intervention, they may survive however many will have varying levels of disability which may alter their quality of life. To understand the impact of IBA, we must also understand Secondary Traumatic Brain Injury. In patients who have sustained a severe head injury, a cascade of events occurs that further damages neuronal tissue and increases the incidence of morbidity and mortality. Apnoea following head injury contributes to the secondary insults and can accelerate the formation of cerebral oedema, intracranial pressure, ischaemia and death of neuronal tissue - it does this by augmenting the following "secondary insults.": [32] [50] [51]

  • Hypoxia - An apnoeic patient will inherently have a lower PaO2 than a patient who is adequately ventilating. These lower oxygen levels contribute to cerebral ischaemia as the supply of oxygen does not meet the demand. [32] [33] [50] [51]

  • Hypercapnia - Along with being hypoxic, lack of ventilation will prevent the elimination of CO2. This leads to an accumulation of carbon dioxide in the circulation, which can have detrimental effects. Carbon Dioxide is a potent vasodilator - high levels will alter cerebral circulation by vasodilating vessels. [32] This increases cerebral perfusion pressure, however also contributes to increasing intracranial pressure (Munro-Kellie Doctrine). [32] [41]


This leads to poorer outcomes in patients, contributing to death and disability. Furthermore, hypoxic / ischaemic conditions may potentiate the secondary neurotoxic cascade that occurs - ischaemic states may result in neurometabolic disturbances and mitochondrial damage which can produce free radicals, further damaging neuronal tissues. [32]

The flow on effect is huge, and each second help is delayed is another step in the cascade leading towards death.

What interventions are important?

In relation to IBA, the two key interventions are Airway Management and Ventilatory Support.

Airway Management

Simple interventions can save lives. Optimizing airway positioning is key - in most circumstances (due to the mechanism of injury and potential cervical spine injury) this will be achieved by a Modified Jaw-thrust. [33]

Airway Adjuncts may be considered. Adjuncts include oropharyngeal airways (OPA), nasopharyngeal airways (NPA), supragllotic airways and endotracheal intubation. [57] [58] It is important to use clinical judgement in these circumstances as these adjuncts can have a detrimental effect. Avoid OPA in head injuries as they may elicit a gag response. [32] [57] [58] [59] NPAs may be considered in head injured patients who are not ventilating adequately - do not insert in the presence of nasal trauma or middle third facial fractures (use cautiously in patients with a basilar skull fracture). [58] Supraglottic airways may be considered in patients with no gag reflex and patients are likely to be ventilated for an extended period of time (>10 minutes). [57] [58] [59] Endotracheal intubation is a common definitive airway in patients with severe head injury. For specific indications, contraindications and procedures see your institutions guidelines / protocols. [32] [57] [58] [59]


Respiratory Intervention in the form of assisted ventilation is another key aspect to management. [50] [51] Using a bag-valve-mask (BVM), positive pressure ventilations at a rate of 12/ minute (allowing for rise and fall of the chest)  should be initiated. This is the most basic level of intervention, and this alone may improve outcomes. [57] [58] [59]

Neuroprotective Ventilation refers to certain parameters which aim to avoid secondary insults and prevent further brain damage. [57] [58] [59]These parameters include:

  • Ventilations at a rate of 12/min [59]

  • Tidal Volume of 6-7mL/kg [59]

  • SPO2 of >95% [59]

  • ETCO2 maintained between 30-35mmHg [59]


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Impact Brain Apnoea occurs with any concussive brain injury and is proportional to the force transmitted to the brain stem.

Primary Brain Injury occurs at the time of injury, and cannot be augmented by medical care.


Secondary Brain Injury occurs following injury, and can be prevented through timely and appropriate care.




Rapid assessment and recognition is key to survival and recovery in these patients.

Once recognised, early respiratory intervention is needed to improve outcomes and reduce mortality.

TBI is still one of the leading causes of morbidity and mortality globally.

Impact Brain Apnoea should be considered a preventable and reverisble cause of cardiovascular collapse in trauma.


Additional Resources

Atkinson J. The Neglected Prehospital Phase of Head Injury: Apnea and Catecholamine Surge. Mayo Clinic Proceedings 2000 ;75(1):37-47. Available from: https://www.mayoclinicproceedings.org/article/S0025-6196(11)64254-7/fulltext

Wilson M, Hinds J, Grier G, Burns B, Carley S, Davies G. Impact brain apnoea – A forgotten cause of cardiovascular collapse in trauma. Resuscitation . 2016 ;105:52-58. Available from: https://traumarummet.files.wordpress.com/2016/06/impact-brain-apnoea-e28093-a-forgotten-cause-of-cardiovascular-collapse-in-trauma.pdf



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