At approximately 07H00 Ubuntu Aeromedical Service received a call on their rotor-wing platform for a young gentleman who had fallen from a height of approximately 5 meters. They were told that the incident had occurred at 06H00, and that the patient was standing on the trailer of a truck when it suddenly moved forward, causing him to fall off of the back end, head-first onto the concrete floor.
On arrival (09H55), they found the patient with typical signs of a severe traumatic brain injury: GCS of 4/15, Cheyne-Stokes breathing, signs of a basal skull fracture, a combination of Le Forte fractures and sluggishly reactive pupils which were equal in size. However, the patient also showed signs of severe decompensated hypovolaemic shock with a low blood pressure (63/51), pale, mottled, cold and clammy skin, and a delayed capillary refill time.
One would have expected to see a ‘Cushing’s response’ to the raised intracranial pressure consequent upon the severe traumatic brain injury (a well-perfused patient with hypertension and bradycardia). So, what happened here – how does one explain this paradoxical clinical presentation?
Shortly after the assessment of the patient was completed, the decision was made to intubate using rapid sequence intubation. However, during preparation for intubation, the patient deteriorated rapidly, went into cardiac arrest. After resuscitation attempts proved futile, the patient was declared dead on scene. The treating paramedic then decided to consult with the Continuous Quality Improvement department at Ubuntu Aeromedical Service, to gain clarity about the conflicting clinical signs in this mystifying “isolated” traumatic brain injury [about this extraordinarily complicated case].
An autopsy was later performed on the patient which revealed the following: confirmed base of skull fracture, intracerebral haemorrhage, pulmonary and cardiac contusions and massive bleeding within the thoracic cavity. Together, these post-mortem diagnoses paint a pretty grim picture. So the prevailing question is: what on earth happened in the chest cavity to cause such a catastrophic bleed? The answer might be a little surprising, as all that bleeding might have resulted from the traumatic failure of a single ligament, the ligamentum arteriosum.
During our foetal development the ductus arteriosus, which links the distal distal aortic arch to the pulmonary artery, is a conduit to shunt blood away from the pulmonary circulation into the systemic circulation. While in utero, oxygenation does not occur in the foetal lungs. But rather, oxygenated blood is delivered to the foetus from the mother, through the placenta and umbilical cord, before being introduced into the inferior vena cava. The ductus arteriosus serves a vital function, as perfusing the lungs when they are not being oxygenated would be fairly pointless.
After birth, the ductus arteriosus begins to close as soon as the neonate breaths spontaneously and blood is once again reintroduced into the pulmonary circulation. Over time, the ductus arteriosus undergoes a transformation from endothelial tissue to fibrous tissue, at which point it becomes known as the ligamentum arteriosum. The ligamentum arteriosum is a fixed structure which forms a ‘tether’ between the aortic isthmus and pulmonary artery.
The distal part of the aorta (as it becomes the thoracic and abdominal aorta) is a relatively mobile and ‘heavy’ structure as it is filled with a large amount of blood. Similarly, the proximal aorta behaves much in the same way, in that it is relatively mobile in comparison to the aortic arch, where it is secured by the ligamentum arteriosum.
During rapid acceleration/deceleration injuries such as motor vehicle accidents or falls from height, the mobile sites of the aorta begin to move in response to the injury, whilst the relatively fixed (or immobile) ligamentum arteriosum prevents the aortic arch from moving. This causes a tremendous shearing force on the aortic wall, and can lead to severe damage of the aortic lining as the ligamentum arteriosum tears out of the aortic wall – and in severe cases results in aortic wall rupture. A rupture of the aorta will lead to massive bleeding within the thoracic cavity, much like was seen in the patient discussed above.
A few numbers
Motor vehicle accidents and falls from height are the two most common causes for traumatic aortic rupture, followed by pedestrian vehicle accidents and crush injuries. Around 0.5% – 2% of all non-lethal motor vehicle collisions and 10% to 20% of all high-speed deceleration fatalities cause traumatic aortic rupture. When you consider these figures, the diagnosis of traumatic aortic rupture carries a considerable risk of mortality, and is immediately lethal in 80% – 90% of cases. However, in contrast to these morbid figures, if aortic rupture was detected in time and the patient was taken to a suitable hospital with sufficient surgical capabilities, the survival rate following definitive care is 60% – 80%. Therefore, prompt recognition and definitive treatment of these injuries are paramount for survival.
Identification and Diagnosis
So now to the nitty gritty, how do we identify and diagnose traumatic aortic rupture? Unfortunately diagnosis would be close to impossible in the field, with signs and symptoms too unspecific to indicate traumatic aortic rupture, apart from severe hypovolemic shock. However, practitioners in the field should keep a high index of suspicion in cases where rapid acceleration/deceleration has occurred. Radiological investigations seem to be the most useful at diagnosing traumatic aortic rupture.
Chest X-rays offer limited diagnostic value, as they can often appear close to or completely normal in traumatic aortic rupture. Evaluation for mediastinal haematoma, and by inference a major vascular injury, is the main goal of initial chest radiograph. Mediastinal widening greater than 8cm and/or 25% of the width of the thorax is the most frequent observation. However, it may not always be the most sensitive finding. More discriminating findings include any abnormality of the transverse aortic arch or loss of the aortopulmonary window. Therefore, even in those cases where the mediastinum is not widened, obscuration of the lung interface with the transverse or descending thoracic aorta should still be viewed with suspicion.
Computerised Tomography (or CT) scans are extremely useful for identifying and diagnosing traumatic aortic rupture as their contrasts between solid (tissues), fluid and gases are much clearer than chest X-rays. They offer a clear view of the continuity of the intima in the aorta, and ruptures or tears or easily visible.
When one considers the complexity of this case, where a severe traumatic brain injury presented together with catastrophic hypovolemic shock, it is understandable that the patient’s prognosis was very poor from the outset. However, the initial delay of an hour in activating the rotor-wing aircraft and crew, together with delays in arriving at the scene, meant that the patient had a three hour window where definitive care could have been potentially life-saving. As mentioned above, a high index of suspicion, early identification and definitive treatment are key factors to improve survival rates, and although these injuries can be immediately fatal in many instances, the survivors have a good chance of recovery if given prompt definitive care.
Pierre Smit is a flight paramedic in Cape Town South Africa who has recently completed his MPhil: Emergency Medicine at the University of Cape Town.
In his own words: “I am a passionate, fun-loving person with a desire to be as involved in Emergency Medicine education as I possibly can. I have high hopes for developing critical care in South Africa for the pre-hospital setting in the coming years, which is a goal I strive towards every day. I am also an avid Mountain-biker and adventure-videographer with the old fractures and scars to prove it.”