a 62 year old female is bought into your ED following a high-speed MVA. She has driven her car into telegraph pole at ~ 80km/hr.
She is haemodynamically stable, with an unremarkable primary survey. Of note, she has an obvious seat-belt abrasion over her anterior chest with significant sternal tenderness on palpation.
This is her mobile CXR taken in the resus-bay….
Clearly her chest x-ray is abnormal. Whilst it is a poor inspiratory film [& the patient is supine], there is an abnormal mediastinal contour which is markedly widened. The trachea is also deviated to the right side.
In the setting of a moderate deceleration mechanism, this raises the suspicion of a blunt aortic injury. She needs to get to CT quickly…
In the meantime;
- Two large-bore IVs are sited
- Fentanyl administered for analgesia
- EFAST performed: difficult study 2* to habitus. Possible LUQ free fluid.
Within the next 10 minutes she is transported to radiology for a CT ‘pan scan’….
So let’s have a closer look…
So let’s have a closer look…
… with a pulse rate of 66 per minute & a blood pressure of 172/98.
What are you going to do now ?!?
This is a trauma patient with a blunt aortic injury. Extrapolating from the non-traumatic aortic dissections, you recognise the importance of both heart rate and blood pressure control in this scenario however cannot help but question the role of β-blockers & vasodilators in a patient with pelvic fractures & an equivocal FAST scan.
Against better judgement you commence a sodium nitroprusside infusion…
TRAUMATIC AORTIC DISSECTION.
Blunt aortic injury is the second most common cause of death from blunt trauma following head injury.
The classic teaching of traumatic aortic injury is that it carries a dismal prognosis; that is 90% die at the scene and of the remaining 10%, 50% die within 24 hour and 90% will be dead within 4 months !! It is It is important to recognise that this data originates from the 1950’s and now with the advent of endoluminal repairs one would expect better survival rates…
Current numbers suggest;
- 50% of aortic injuries will rupture within 24 hours (~80% within the 1st week)
- Overall mortality for those surviving to hospital evaluation is ~31%.
The most common location of injury is the aortic isthmus, accounting for 75-95% of cases. Whilst the aorta can be injured directly, there are several theories of various indirect forces resulting in aortic injury;
- During deceleration the mobile heart & ascending aorta swing forward and can result in intimal tearing at the isthmus, where the descending aorta is fixed to the posterior chest wall.
- Sudden rise in intraabdominal pressure creates a water-hammer effect within the aorta.
- Osseous pinch results in entrapment of the aorta between the anterior chest wall & the vertebral column.
For more information on Aortic Dissection, especially clinical features, diagnostic tools and management – check out thebluntdissection – chest pain and… !!
WHEN SHOULD WE SUSPECT THIS INJURY ?
Blunt aortic injury most often occurs after sudden deceleration, typically motor vehicle accidents (72% from ‘head-on’ collisions). Other causes include;
- motor cycle or aircraft crashes
- especially unrestrained drivers or ejected passengers.
- pedestrian vs car
- falls (>10 feet, 3 meters)
- crush or compression injury
- Chest (± back) pain
- 1st & 2nd rib fractures or sternal fracture
- Multiple rib fractures (or flail chest)
- Posterior displaced clavicle fracture
- Brachial plexus injury
- Palpable supraclavicular mass
- Unexplained chest haematoma
- Blood pressure differentials or pulse deficit
RADIOLOGICALLY (Chest Xray).
- Widened mediastinum (>8cm)
- Mediastinal/chest width ratio > 0.38
- Obscured aortic knob
- Depressed left main bronchus
- Large haemothorax
- Opacification of aorto-pulmonary window
- Widened paratracheal & paraspinous stripes
- Left apical cap
- NG tube deviation
- 1st or 2nd rib fractures
- Multiple rib fractures
- Sternal fracture
- Posteriorly displaced clavicle fracture
Once the diagnosis is made, treatment must be timed properly. Whilst immediate operative repair used to be the rule, several studies now support a delayed repair with tight haemodynamic control especially with coexisting traumatic injuries such as head injury, exsanguinating bleeding, pelvic injuries or lung injury. The following table highlights this decision process;
In the unstable patient, management focuses on concomitant resuscitation whilst detecting and correcting the underlying cause of haemorrhage. It is important however, to avoid over resuscitation.
Careful, meticulous blood pressure control is mandatory until definitive surgical repair can be performed. If operative repair is delayed, then systolic blood pressure should be corrected to 100-120 mmHg.
Whilst there are many feasible ways of doing this (depending on available medications & local practices), the key is to avoid rebound tachycardia which can increase shear stress on the intimal flap (ie. lowering the dP/dT). Therefore beta-blockers are often utilised with the vasodilator agent (eg. esmolol + nitroprusside), aiming for a pulse rate of 60 per minute.
SURGICAL vs ENDOVASCULAR REPAIR.
Open surgical repair is usually indicated for;
- Haemodynamic instability
- Large-volume haemorrhage from chest tubes
- Contrast extravasation on CT (or rapidly expanding mediastinal haematoma)
- Penetrating aortic injury
Endovascular repair has documented benefits such as reduced blood loss, minimally invasive approach, allowance for neuroprotective positioning and reduction in rates of paraplegia. A significant limitation at present is, if the aortic injury occurs adjacent to a sharp bend the graft may provide poor apposition and risks device collapse. Proximity to the left subclavian artery can also result in ischaemia and care must be taken in those with a dominant left vertebral circulation.
… with the nitroprusside infusion trickling in her blood pressure gradually drifts down to 120 mmHg systolic !! Interestingly her pulse rate does not budge & you wonder if she is pre-morbidly beta-blocked. This was not clarified at the time due to language barrier.
Behind the scenes, arrangements are made with Interventional Radiology and Vascular Surgery to proceed to the angiography suite.
Here are her images…
Following an uneventful procedure, she is transferred to Intensive Care for ongoing observation and tight blood pressure control.
Here is her CXR on day 2…
She continues to make a slow but steady recovery….
- Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
- Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
- Parmley, L. F., et al. (1958). Nonpenetrating traumatic injury of the aorta. Circulation, 17(6), 1086–1101. doi:10.1161/01.CIR.17.6.1086
- Dosios, T. J., Salemis, N., Angouras, D., & Nonas, E. (2000). Blunt and penetrating trauma of the thoracic aorta and aortic arch branches: an autopsy study. The Journal of Trauma: Injury, Infection, and Critical Care, 49(4), 696–703.
- Reed KC & Curtis LA. Aortic Emergencies – Part II: Abdominal Aneurysms And Aortic Trauma. Emergency Medicine Practice. 2006; Volume 8, Number 3.
- Nagy, K., Fabian, T., Rodman, G., Fulda, G., Rodriguez, A., & Mirvis, S. (2000, June). Guidelines for the diagnosis and management of blunt aortic injury: an EAST Practice Management Guidelines Work Group. The Journal of Trauma: Injury, Infection, and Critical Care. 48(6): 1128-43.
- Fabian TC, Davis KA, Gavant ML,et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998;227:666-76
- Traumatic Aortic Injury – trauma.org