EMCrit.org

Aortic Injuries

Traumatic Aortic Disruption (TAD)

 

Aortic Rupture

Arch is mobile just distal to L subclavian

Can also tear major branches

Secondary to trauma, cpr, t-spine fx

Suspect if deceleration injury or side impact mva, fall >30 feet, steering column or wheel damage.

Chest CT-may give false positive c mediastinal hematoma, necessitates aortogram

TEE-better

Aortogram-gold standard

Proximal Descending-most common

Ascending-80% have associated cardiac injuries

Manage c esmolol then nitroprusside

Can get spinal cord ischemia and atrial-aortic fistulas

ABD CT

If L hemothorax is seen or periaortic hematoma, strongly consider thoracic dissection/rupture (J Trauma 52 (4):699 2002)

 

Most recent review supporting helical CT (Emerg Med J 2004; 21:414-419)

Best study to date of CTA for aortic injury shock trauma (J Trauma. 1998 Nov;45(5):922-30)

 

 

Chest X-ray

Best study (274 patients)

(Fabian T. J Trauma 1997; 42: 374-383)

Wide mediastinum
221
85%
Indistinct aortic knob
63
24%
Left pleural effusion
49
19%
Apical cap
49
19%
Tracheal deviation
32
12%
NGT deviation
29
11%
Bronchus deviation
12
5%
Normal chest X-ray
19
7%

X-Ray (90-95% sensitive)

Increased mediastinal width >8 cm at knob

Indistinct arch

Opacification of space between aorta and pa

Deviation of NGT

Widened paratracheal stripe

Depression of L mainstem

L apical pleural cap

All chest x-ray findings are of mediastinal hematoma which is not the same thing as TAD.  10-20% of mediastinal hematomas will turn out to be TADs.  Massive hemothorax is the only direct sign of TAD on C-XR.

 

Most recent study casts doubts on utility of supine chest film (J Trauma 2004;56:243)

 

Chest x ray did not show obvious mediastinal widening, but incidentally the space between intimal calcification and the outer border of the aortic arch was >1 cm, a recognised radiological sign of aortic dissection (fig 1Go). Awareness of this is crucial. Troponin was normal but D-dimer was raised. A computed tomography scan confirmed aortic dissection type B, managed conservatively with intravenous labetolol and analgesia, with a good outcome. ( Gartland et al. 24 (4): 310 -- Emergency Medicine Journal)

Helical CT in TAD

Author
Total
TAD
Sensitivity
NPV
Fabian
J Trauma 98
494
71
100%
100%
Mirvis
J Trauma 98
1,104
24
100%
100%
Dyer
J Trauma 02
1,338
30
100%
100%

 

Signs of TAD on Helical CT

Direct

Well visualized flap

false lumen with flow

obvious aortic disruption

Indirect

mediastinal hematoma

abnormal vessel contours

question of flap on one cut

 

Most Recent J Trauma Study (Volume 56(2)   February 2004  pp 243-250) One center states CT ready for prime time as sole diagnostic test

 

1.    The initial resuscitation should not be aggressive.  Keep the BP below 90/-
2.    NONE should go to CT.  Look at the chest x-ray, mechanism and PE,  If you are suspicious of an injury from these screening tests.  GO TO AORTOGRAM
 
3.    If the mechanism is suggestive, but the Chest X-ray is NOT, then a CT to look for a mediastinal hematoma is indicated.  FOR ANY PATIENT WHO YOU ARE GOING THROUGH ALL THESE EVALUATIONS, THEY SHOULD BE ON BETA BLOCKERS UNTIL DX IS RULED OUT OR OPERATION IS COMPLETED
 
4.  Only ones to go straigtht to OR are those who are unstable.  Stable patients should wait till daylight or up to 3 days acutely if they have extensive associated injury.   
 
5.    CT is a screening NOT DIAGNOSTIC aid.  I know of NO case I have seen in the hospital, or those I have seen in consultation in the court room that the CT ALTERED ANYONES DECISION MAKING.   I AM FAMILIAR WITH FAR TOO MANY CASES THAT THE CT AND TEE were misleading and led to spurious decision making.  
 
 
The ATLS does not address the urgency for operation.  You will find that in the thoracic surgery and trauma literature. 

Delayed Treatment

It may be an acceptable strategy to stage the injury and then perform delayed repair with interim lowering of BP and HR.

Retrospective Study (J Trauma Jan 2004 56:1) use serial c-xrs to check silhouette

Shoot for MAP<70 with b-blockers and then nitrites

 

Pacini D, Angeli E, Fattori R, et al. Traumatic rupture of the thoracic

aorta: ten years of delayed management. J Thor Cardiovasc Surg 2005;

129:880-884.

 

 

The cardiac surgeons of the Massachusetts General Hospital pioneered

the immediate medical and delayed surgical management of patients with

traumatic rupture of the thoracic aorta starting in 1971. Since their initial

report in 1981, several additional series have been published attesting not

only to the feasibility of such management but to the actually improved

outcomes it makes possible. This article from Bologna, Italy, adds to that

collection and contributes a new dimension: a series of patients treated not

only with delayed repair but with endovascular stenting rather than via open

thoracotomy. The charts of 69 patients with traumatic thoracic aortic rupture

seen over 23 years were reviewed. Twenty-one, seen between 1980 and 1993,

were managed with immediate operative repair. Four of these died, and 3

developed paraplegia. Beginning in 1993, patients were treated with initial

medical management, followed by delayed repair. Of these 48, 5 required

urgent repair, 3 via surgery and 2 via endovascular stent placement.

Indications for urgent repair were massive hemothorax and contrast

extravasation on CT, rapid enlargement of the pseudoaneurysm, and

pseudocoarctation. The remaining 43 had delayed repair, 13 with an

endovascular stent and 30 via open surgery. Only 2 of these patients died,

and only 1 developed paraplegia. All 15 stent placements were successful and

uncomplicated. This is real progress and is certainly the direction of

the future.

 

 

Graft Infection

 

 

Patients who need to be transferred to other facilities for definitive repair
Severe head injury
Severe pulmonary injury
Haemodynamically unstable patients
Patients who have undergone damage control procedures
Patients with coagulopathy, hypothermia & acidosis
Patients with severe medical co-morbidities
Patients with burns or severe sepsis.

 

(2) decrease of the rate of the arterial pulse increase (dP/dt) to diminish shearing forces.

 

The use of beta-adrenergic blockers (β-blockers) is the cornerstone of aortic dissection management. Because nitroprusside increases the heart rate and may also increase the dP/dt, a β-blocker must be started before or in conjunction with sodium nitroprusside to lower the dP/dt. Esmolol is an ultrashort-acting β-blocker that is easily titrated. After mixing 5 g in 500 ml D5W, an initial bolus of 500 μg/kg is given, followed by an infusion of 50 to 200 μg/kg/min. Labetalol has both α-blocking and β-blocking activity and can be used as monotherapy. A suggested dose is an initial 20 mg IV bolus every 5 to 10 minutes, incrementally increased to 80 mg until a target heart rate has been reached or a total of 300 mg is given. A maintenance dose of labetalol is then given at 1 to 2 mg/hr. A target heart rate should be between 60 and 80 beats/min. If a patient is normotensive, a β-blocker should still be used to lower the dP/dt.

 

Trimethaphan is mixed as a solution of 500 mg in 500 ml D5W and is infused at a rate of 1 to 2 mg/min. Trimethaphan is a ganglionic blocker that reduces both arterial pressure and its rate of increase, thus not requiring the use of concomitant β-blockade. It is more difficult, however, to titrate trimethaphan than to titrate nitroprusside, and tachyphylaxis frequently occurs after 24 to 48 hours.[46] Additionally, the frequency and severity of side effects (e.g., respiratory depression, nausea, urinary retention) limit the use of trimethaphan.

 

 

I guess this myth persists still, Karim--in fact ANY patient can get a pretty near-to-uprite film if we want one regardless of their potential injuries or status.  You do not have to sit the patient up , that is, bend at the waist , to do this--it is quite easy to put the stretcher in reverse Trendelenberg position, putting the body fairly uprite while keeping the body straight in alignment and shooting the film perpendicular to the body axis--we do this often, there are papers written on it from years back showing its value--we seem to continually forget.

 

Joseph Ayella, the original trauma radiologist at Maryland Shock Trauma, 
described this technique.
 
The xray beam must be about ten degrees toward the feet to obtain a 
"pseudoupright" film. If the patient is completely upright, then you must  increase
the angle of the xray source. However, you must get the patient  somewhat
upright so that the xray source can be directed horizontally in stead  of the
vertical position for a supine film.
 
The value of this technique is that it allows the technologist to increase 
the film/xray source distance to 72 inches which reduces magnification. The 
angle allows a proper projection of the mediastinum. The xray source can only go
 vertically about 40 inches.
 
However, lest i be seen as a die hard advocate of this technique, I would 
not do it in an unconscious patient or in situations of possible spine 
instability. Not worth the risk and those patients all have to go to CT anyway,  So we
can get a better idea of mediastinal width, hemorrhage etc from the  CT